THE EVOLUTION OF MENTAL HEALTH.

     The Evolution of Mental Health proposes that mental illness is an avoidable terminal state consequent upon spending one's formative years without the conditions necessary for one's mental health to evolve. An illness or a disease is an interruption to a normal life, and it has an identifiable anatomy and an identifiable pathology: mental illness in conventional terms does not meet these criteria.
     Parents and teachers have an instinct about what mental health is, but often they do not realise that they have this instinct. As evidenced by the lack of any working clinical definition of mental health, doctors and university psychiatrists do not have an instinct about what mental health is, and often they do not realise that they do not have this instinct, all of which is consequent upon the considerable inhibition of instincts necessary to qualify as a doctor and to succeed as a university psychiatrist. Hospital psychiatrists have an opportunity to unlearn the inhibitions learned at medical school.  

     The evolution of humans has included the assumption of an erect posture, with consequent increases in visual and auditory brain circuitry at the expense of olfactory brain circuitry. The less instinctual forebrain has expanded at the expense of the more instinctual hindbrain. The loss of instinctual brain means that the cultivation of instincts is likely to be a more delicate and complicated process for a human than for a quadrupedal carnivore.
     The longer that an offspring is dependent on its parents, then the more that offspring is reliant on those parents for the cultivation of its instincts, and thus for its awareness of itself.

     Awareness of his or her instincts is one of the conditions necessary for a child's mental health to evolve. Another condition is that the child's instincts are reflected back to the child visibly and audibly through responses of the parent or carer, so that connections are developed between the child's instinctual brain and the child's perceptual brain.
     Instincts are remembered. Instincts that are reflected back are remembered. Instincts that are not reflected back are remembered. Connections developed between reflected instincts and the immediate visible and audible world are remembered.
     A child who does not experience his or her instincts as reflected by others may prefer to remain in an autistic world, wherein his or her instincts reverberate without reference to others, and wherein the child can talk his or her own language.
     Schizophrenia occurs because of the accumulation during childhood of some unreflected instincts, which then erupt during adolescence under the influence of hormonal changes.
     Mood disorders occur because the instinctually developed child does not learn how to reflect on his or her instincts personally, but remains dependent for those reflections on an adult, in whose absence there are feelings of loss and a driven, uncultivated attempt to cope.

     The evolution of the mental health of a child in the human habitat has parallels with evolution in general. If mental health is defined as the capacity to review independently one's mental state as it is perceived by others, then this can be construed as a particular example of homeostasis, in that the perception by others is an environmental change, and the review is made with an intention to vary one's personal responses if one chooses. Experimentation with instincts occurs in the harmless, ritual fights of animals and in the play of children. A prey is more likely to survive an exchange with a predator if it locates itself in the predator's visual and auditory world, and if it remembers previous exchanges. Children who feel isolated and threatened in their human habitat may use mimicry and crypsis to survive. Parents have to inhibit their own predatory instincts if they want their offspring to develop.
     Both females and males have the hormone prolactin, which stimulates milk production in females, and the hormone oxytocin, which produces uterine muscle contraction and milk ejection in females. The Royal Society has described how an injection of oxytocin has made a wild social mammal more cooperative, which would be an important link in the evolution of mental health, if it were true.
     Connections developed between the instinctual brain and the perceptual brain can be delineated in potentially disprovable cellular circuits; this is a specialist subject which is therefore in small type.

     Evolutionary issues have not been within the range of university psychiatry, which has tried hard to be objective, but which has failed to grasp that objectivity and emotional detatchment are not the same thing. That is why it did not occur to Kendell et al. that their unexpected findings with patients (354, page 126) were due to what was going on inside their own heads (3), and that is why researchers and journal editors remain incapable of addressing the emotional advantages inherent in the fantasy that studies are "double-blind" because they say that they are (10) (1638) (2387) (644) (2457) (2567) (2568) (2659) (2728) (1766) (2738) (1615) (2692) (2693). Reference (10) was published by the editor of the British Journal of Psychiatry, Hugh Freeman, only after the threat of a media exposé. These examples, and the widespread use of verbalisation without vocalisation (P), attest to how university psychiatry has lost its instinctual brain, and is very much the psychiatry of the forebrain. Given that all of these examples have been in the public domain for decades, it is evident that university psychiatrists have exercised choice over what they have attempted to disprove.

     Having cut itself off from basic instincts through emotional detatchment, university psychiatry has cut itself off from scientific issues like evolution and homeostasis about which it ought to be making major contributions. There are other examples. If the theory of inclusive fitness means that members of nuclear families propagate their genes by being nice to each other, then this needs to be set against the stark realities of the psychiatric consulting room, in that the members of nuclear families can be absolutely beastly to one another, with the consequences of celibacy and of conventional mental illness. Again, a proponent of any theory of language needs to be seen to address the social through to cellular differences between the statements "I see you." and "I see you seeing me.". Also, genes exist in a genetic environment, which differs between individuals. University psychiatry is a narcissistic celebration of the Y chromosome.

     The Evolution of Mental Health explores some understated areas of university psychiatry, for example the degree to which our mental health arises out of our animal ancestry, specifically out of the interplay between our animal instincts, mediated by the diffuse reticular network and by the amygdalae, and those centrifugal inhibitions, mediated by the cerebral cortex, that are necessary for the habitat and the territory to be workable. This exploration concludes, for example, that an hallucination is not a perception without an external stimulus, it is an apperception without an internal stimulus.
     The Evolution of Mental Health emphasises that the investigation of mental illness should include all the members of the human habitat, and not just the notional "patient". If, as we are told so often, mental illness has a genetic basis, then what are the environmental factors that enable the perpetuation of those genes? One obvious, albeit disagreeable, possibility is the protection of the senior members of the human habitat at the expense of the relatively defenceless junior members. Blood may be thicker than water, but it is not thicker than sperm. The failure to investigate parents thoroughly is exemplified by research into developmental disorders. The necessary experimental designs are spelt out in The Evolution of Mental Health. On which percentiles are the parents on a graph of parental perception of their child's ∂x/∂t, where x is vocal frequency or vocal intensity, and t is time? How much of the parents' language is adjusted to the ages of their children when it is analysed by frequency and intensity?
     The opening of doors requires a commensurate opening of minds. Community care will only be effective in the long term if it operates before the damage is done, and not just afterwards. This will require a greater degree of introspective exactitude from desperate parents and expedient general practitioners than has obtained hitherto, but they are unlikely to defer to an apologist profession which knows that it has embodied introspective inexactitude, specifically the failure of its clinicians to place the same emphasis on vocalisation (2838) as they place on verbalisation in the measurement and classification of psychiatric symptoms, the failure to put a screen in between supposedly independent diagnosticians so that they can't cog, and the failure to have a standard test of knowledge of treatment allocation in drug trials; and the failures of its professors and editors to direct research so that differential calculus is applied to the endoderm of the larynx with the same enthusiasm as it is applied to the ectoderm of the scalp, so that the outmoded and discredited concept of the limbic system is replaced by recognition of the difference between allocortex, mesocortex and neocortex and of the different vectors between the cell layers of those cortices, so that the anatomical reality of the diffuse reticular network of nerves is incorporated into models of mental illness, and so that the subject matter of psychiatry is used to apply the concept of homeostasis across humans.
     One of the functions of university psychiatry is to defend orthodoxy, as indicated by the above failures to attempt disproof of possibilities that would threaten orthodoxy, and this has contributed to the evolution of mental illness.
     The evolution of schizophrenia in conventional terms occurs because ontogeny does not recapitulate phylogeny, in that a family divides labour so as to increase its fitness at the expense of one of its members, who is thereby consigned to an extreme discrepancy between phenotype and genotype, the latter expressed as a distinctive set of relationships within and between pairs of reciprocal genes, configured during parental meiosis and then during fertilisation. The consequence is a human being who has a detailed map of the world, but who does not have the capacity to find himself or herself in it.
     It is an instructive nemesis that some aspects of the diagnosis and treatment of mental illness stigmatise the medical profession.

The text in larger type provides a general commentary, while the text in smaller type deals with more specialised issues. Text in quotation marks that is not followed by a reference number is notional.

Please click on any of the following underlined terms:

Mental illness diagnosis. Schizophrenia. Delusions. Hallucinations. Depression. Mania. Headache. Mental Health.

MENTAL ILLNESS TODAY.

     Diagnosis: unreliable.

     Treatment: the "double-blind" lead the "double-blind".

     Research: grammar is an excellent guide to the substance of research studies.

     Prevention: mental health is the absence of mental illness.

A QUICK GUIDE TO THE DEVELOPMENT OF MENTAL ILLNESS.

THE STRUCTURE AND FUNCTION OF THE BRAIN.

     General outline, with a notional example.

     The cerebral hemispheres.

     The cerebellar hemsipheres.

     The basal ganglia.

     The thalami.

     Hypothalamic structures.

     The brainstem.

     The spinal cord.

     Brain cells.

     Genes.

A DETAILED GUIDE TO THE DEVELOPMENT OF MENTAL ILLNESS.

     The frontal lobe.

     A split in the brain: schizophrenia.

     Vulnerability to loss: mood disorders.

ADULT ADJUSTMENT.

A QUICK GUIDE TO THE PREVENTION OF MENTAL ILLNESS.

EVOLUTIONARY THEORIES AND MENTAL ILLNESS.

ETYMOLOGY.

REFERENCES.


MENTAL ILLNESS TODAY

          Diagnosis: unreliable.

     Medical diagnoses of mental illness may have a degree of truth, but they are unlikely to be the whole truth, and spurious claims of high levels of agreement between psychiatrists have meant that they have not been nothing but the truth.

     Something approaching the whole truth can be ascertained by reference to the International Statistical Classification of Illness and related Health Problems (1), which includes in its chapter XXI, sections Z 61, Z 62 and Z 63 respectively, problems related to negative events in childhood, problems related to upbringing, and problems related to the primary support group, including family circumstances. However, these problems rarely seem to be used in formal communications about the patients, who, all too often, are referred to by metonyms like "schizophrenic" (2519).

     Psychiatrists use terms like "schizophrenia" and "manic-depression", but in England these have not been supported by inclusion in the Mental Health Act of 1983 (2). The justification for such terms seems to be high levels of agreement about symptoms between pairs of psychiatrists who assess patients simultaneously. Tellingly, the levels of agreement about signs are unremarkable. Symptoms such as: "Have you been feeling depressed?" are based on questions and answers, whereas signs such as: "Does the patient look sad?" are assessed silently. Therefore, the high levels of agreement about symptoms could occur because the psychiatrists can both see and hear each other, and thus are able to pick up cues from one another about how each is going to rate the symptom in question, whereas the unremarkable levels of agreement about signs occur because the psychiatrists merely see each other in silence, and so are unable to pick up cues about their respective ratings because neither psychiatrist knows which sign is being rated by the other psychiatrist at any moment. The interposition of a screen between the two psychiatrists has been followed by a fall in the high levels of agreement about symptoms to the same unremarkable levels of agreement as about signs, which levels have been unaffected by the interposition of the screen (3). This critique needs to be met, and needs to be seen to be met, by those who wish to represent medical diagnoses of mental illness as having consensus, over and above what might be produced by a communication network (R, pages 182-198) (M) (2643). This is a variant of the "cahoots" hypothesis, described in studies of agreement about personality (319) (1574) (320).

     The fantasy that psychiatrists are machines and not people is seen currently as a presumption that if a high level of agreement about symptoms has been achieved with a particular interview by one group of psychiatrists at one point in time, then this high level of agreement can be assumed to hold for other groups of psychiatrists and for other times, using the same interview (4) (5) (6). The degree to which the initial high level of agreement about symptoms was situational has been ignored (3) (1931). Some of these results are being compared with neuroimages, notionally to advance diagnostic knowledge (6). The money would be better spent on sequential neuroimages of patients as they enter care and then receive treatment, without the unassuaged loss of individuality consequent upon psychiatric diagnosis, and upon the averaging of data across subjects (410).

     Neuroimages are a great advance (1348) (1360) (1617) (1667) (1964) (2148) (2412) (2752) (2859) (2873), provided the experimenters acknowledge the effects on brain images of technical variations (1970) (2059) (2676) (2691); of individual variation (1800) (2023); of observer bias (1118); of design bias (1561) (1784); of personality (652), with consequent use of change measures (269) (298) (512), or of performance controls (1692); of movement, both within and between (407) scans, and of muscle tone, which latter might, for example, explain differences between negative feedback and positive feedback, and between degrees of uncertainty (316); and of the degree of disclosure of the experimental design, given that the brain distinguishes clearly between knowing what it knows and knowing what it does not know (394), as well as between knowing what it knows and not knowing what it knows (980) (1131) (1132) (1178) (1737). If the explicit task for the subjects is different from the actual task addressed by the experimenters (299) (1892) (2332), the subjects may feel deceived (R, pages 245-255, and pages 279-290), which feelings may then affect their brain images (300). Any experimental design that requires the subjects to be misled needs to be seen to be tested as to its success after the experiment, thereby to allow the results to be interpreted in an ambience devoid of experimenter omnipotence. The act of having misled the subjects needs to be seen to be discussed as part of the debrief after the experiment.
     Neuroimaging studies of developmental disorders should address the actual relationships between the patient and his or her parents (1669) (2362), and not just study the patient (1663), or the patient in relation to derivatives (1685), or in relation to controls (1686) (1687). The predictions to be disproved are that there will be less activation of identical areas of the brains of children with developmental disorders and the brains of their parents than between the brains of normal children and the brains of their parents, not only when the child's responses follow the parent's responses, but also when the parent's responses follow the child's responses (1739); that the differences between the brains of parents of children with developmental disorders and the brains of their children persist when those parents are studied with normal children, and that the differences between the brains of children with developmental disorders and the brains of their parents reduce when those children are studied with the parents of normal children; and that the brains of the parents of children with developmental disorders show less activation of the medial side of the cerebral hemisphere in general, and of the cingulate lobes in particular, than the brains of parents of normal children, during joint responses.
     Subcortical structures have been studied (1204) (1147) (2388).
     Neuroimages have distinguished between the production of nouns and verbs (496).
     The results of an experiment about neuroimages should include description of both activations and deactivations (410) (512) (269) (769), mindful of the uncertainties about baseline brain function (1985) (2214); (2188) (2367); (408) (526) (1910) (2131) (2147) (2197) (2511) (2530) (2596) (2733) (2846).
     Neuroimages will be at their most powerful if their spatial sensitivity is combined with the temporal sensitivity of electroencephalography (962) (463) (480) (1859) (2160) (2197) (2216) (2279) (2369) (2534) (2552) (2599).

     The pretence that diagnoses of mental illness contain more of the truth than is in fact the case discourages patients and their families from their own natural attempts to explain what has happened and to do something about it. "You are suffering from the role that you have learned to play within your family" is a very different message from "You have a disease that needs medical treatment." The greatest possible care must be taken, and must be seen to be taken, by the medical profession, not to overstate its case, given that a side-effect of such overstatement is reduction in the patient's autonomy.

     To what degree are mental illnesses social constructs invoked by any society at any time to enable limits and stability, and to what degree are mental illnesses real physical entities that have arisen out of some combination of our genetic inheritance, our personal development and our evolutionary background (607) (608)? From a genetic perspective, the possession of a particular gene has very little predictive value with respect to any mental illness, and the diagnosis of any mental illness has very little predictive value with respect to the possession of a particular gene. From a developmental perspective, brain damage around birth cannot, in itself, explain hallucinations and delusions that make their first appearance in adolescence. The concept of a latent period has not been productive in epilepsy (1032). The lack of a description of mental health makes it difficult to discern the development of mental illness during the formative first decade of life. The paucity of studies of the parents of children with developmental disorders looks weak and defensive (2930). The periodic features of mood disorders cannot be explained by a structural fault alone, and, unsurprisingly, the structural findings have been inconsistent and contradictory (239) (641) (327) (7) (328) (2589) (2886), while at least one of the models has been clinically naive (2483). From an evolutionary perspective, there has been comparatively little attempt by psychiatrists to relate the features of mental illness to animal behaviour (N) (8) (9) (321) (72) (301) (1111) (2080). Some of these deficiencies amount to a lack of scholarship, and feed the suspicion that diagnostic psychiatry is indeed, to some degree, opportunistic, and the lackey of Society's expediency.

          Treatment: the "double-blind" lead the "double-blind".

     One of the ways in which drugs are introduced into psychiatry is on the basis of drug trials, in which the new drug compares favourably with an established drug. Many of these drug trials have what is called a "double-blind" design, which means that neither the patients nor the participant researchers know which patient receives which drug, new or established. However, this design is just that, a design, a plan, and an intention. Whether or not the drug trial turns out to be "double-blind" in practice is an evidentiary matter, necessitating the collection of evidence that can be tested (10). In practice, such evidence is rarely sought, for example (1638) and (2387), so that large numbers of patients are in a position to litigate against the medical profession.

     The lack of a test of the "double-blind" design in drug trials means that it is relatively easy to introduce a new drug into clinical practice, because the trial organisers do not have to address the possibility that the participant researchers were able to make educated guesses as to which patient was receiving which drug, based on the side-effects of the drugs. Once the participant researchers have an inkling about which patient is receiving which drug, they can slant their findings in favour of the drug that they wish to discover (R, pages 152-159), and that the pharmaceutical industry wishes to market (2135). Thus, suppose that after a period of treatment with one or other drug, a patient is asked: "Are you feeling depressed?" and replies: "Well yes. But then again, no." If the researcher suspects that the patient is receiving the established drug, then he or she can develop the "yes" part of the answer and rate no improvement, whereas if the researcher thinks that the patient is receiving the new drug, then he or she can develop the "no" part of the answer and rate improvement. In this way, the new drug can be made to appear superior to the established drug through clandestine knowledge of drug allocation. What ought to happen is that at the end of a "double-blind" drug trial, the participant researchers should be debriefed, and asked to guess the drug allocation of the patients, giving reasons for the guesses.

 Researcher guesses  Correct  Incorrect
Actual 15 5
Chance 10 10

Figure one

The researchers' guesses should then be compared with chance expectation and the results expressed using conventional statistical parlance. For example: "The researchers' guesses were correct, with a probability of one in twenty that this was due to chance..." would indicate that probably the trial had not been "double-blind", because the researchers probably had known which patient was receiving which drug. The reasons given for the guesses would clarify why probably the trial had not been "double-blind", for example, because the researchers had detected a truly superior drug, as in: "I thought that because the patient was so much better than expected, she must have been receiving the new drug...", or, because the researchers had become aware of drug allocation through side-effects, as in: "I suspected that the patient was having the established drug because of his dry mouth...".

     Participant patients should also be debriefed and assessed for knowledge of treatment allocation through guesses, giving reasons for the guesses. It is difficult to see how a trial of intravenous erythropoietin could have been described as having a "double-blind" design when "blood letting" was an expected intervention, which was actually required in eight patients (2090).

     The same test procedures should be used for any supposedly "double-blind" design (644) (2457) (2567) (2568) (2659) (2728) (2860), the moreso if the design requires that every participant uses each of the treatments at different times (1766) (2738) (2812) (2864): comparisons within participants give every participant the opportunity to compare the treatments by any means whatsoever, including appearance, taste, and side-effects, and not just according to the intent of the experimenter, by treatment effects.

     The preparations used in drug trials should be tested for comparability before the trial, and the results should be included in the report, rather than having to be elicited by correspondence (2563).

     The medical profession is open to litigation by any patient who is dissatisfied with a prescribed drug that has been introduced on the basis of a "double-blind" drug trial that did not include a test of the "double-blind" design, not just because of what the drug did not do (lack of therapeutic effects), but also because of what the drug did do (side-effects): the decision to risk the side-effects of a drug is based partly on the therapeutic potential of the drug, so that if this has been exaggerated or invented, then the patient may have been exposed pointlessly to the side-effects. The writer has been unable to penetrate the sub-group that is the medical profession with the seemingly mutant idea that signals to patients about drugs need to be more honest (11). Sir Donald Irvine, President of the General Medical Council, and Sir George Alberti, President of the Royal College of Physicians, subverted the implementation of this exactitude, hence this website: intolerance of phenotypic variation augurs extinction. Perhaps there is a fear that the costs of honesty will be too high (12) (2357). But to whom? Currently, the costs of deception are being borne by a relatively small number of the patient sub-group who have moderate to severe depressive illness and who should not, therefore, be given new drugs that have not been properly tested, but who should be given drugs proven by usage; the larger number of the patient sub-group has a mild degree of depressive illness that is below the threshold at which the difference between established, proven drugs and unproven drugs starts to matter. So there is safety in numbers, which gives the appearance that the strategy is evolutionarily stable, which, of course it has been in this instance because it has resisted penetration. The risk is that the stability relies heavily on perceptual error (13), and that if accuracy prevails (580), perhaps due to a change in circumstances (745), such as a scandal, then there will be a very tough question about the degree to which the relationship between the medical profession and the pharmaceutical industry on the one hand, and patients on the other hand, has been more akin to that between a predator and a prey than to that between a parent and an offspring. In the context of the handicap principle (498), the suicidal threats of the sub-group of patients with moderate to severe depression, who have failed to respond to the prescription of improperly tested drugs, can be seen as provoked attempts to improve the authenticity of communication with their doctors, whose prescriptions have said more about the dominance hierarchy between sub-groups, than they have about effective treatments. "Double-blind" drug trials are Inadvertent Social Information about the people who perform them (589) (666), and show, for example, that those people are prepared to participate in a self-fulfilling prophecy, because they behave in ways that make any false description of differences between drugs come true (2482). The increasing use of herbal medicines may reflect insight (343) (344) (1024).
     Trials of equipment have been flawed similarly (1615) (2692) (2693), although there has been at least one exception (2097).
     Science has been complicit, for example (R, page 297) (303) (1913) (2026).
     In 1998, the Lancet published a study that purported to introduce a placebo needle into acupucture research (509). Although the subjects were asked to distinguish the placebo acupuncture from the real acupuncture, and although the subjects who received the real acupuncture before the placebo acupuncture were over three times more likely to feel a dull pain sensation with the real acupuncture (p<0.008, one-tailed test), the entire publication was devoid of tests of statistical significance. This has not prevented the citation of the report in 2006 as evidence of "...a novel placebo intervention, a validated sham acupuncture needle..." (468): one of the other studies cited as validating the sham acupuncture needle actually invalidated it, because 40% of the subjects could tell the difference between the sham acupuncture needle and the real acupunture needle (510).
     In 1998, the Archives of General Psychiatry published a study of bright light treatment of winter depression (983). The patients went to two different buildings to maintain the blindness of the raters . However, the patients knew their treatment allocation, and could have communicated that in either, or both, settings, which necessitated attempted disproof through a formal test of the researchers' awareness of treatment allocation.
     In 2006, the Proceedings of the National Academy of Sciences of the United States of America published a study of melatonin in the treatment of winter depression (999). The experimenters reported that another research group, in a previous study, had shown that melatonin 0.1 mg had been minimally soporific, and indistinguishable from inert filler in otherwise identical placebo capsules (1632). The experimenters did not compare their own capsules of melatonin and placebo systematically, which was opportunistic, because of the presumption that all of the features of the capsules generalised from one study to the other study.
     In 2006, Science published an article that purported to show a double dissociation for the involvement of noradrenaline and serotonin in human cognition (562). No attempt was made to show that the capsules of atomoxetine 60mg, citalopram 30mg or placebo were indistinguishable by the sixty healthy male participants, so that there was a lack of dissociation between the knowledge of an effect and an effect.

     In 2007, the Proceedings of the National Academy of Sciences of the United States of America published:"A double-blind randomized placebo-controlled phase III study of a Pseudomonas aeruginosa flagella vaccine in cystic fibrosis patients." (2385). A total of 318 adverse events were registered during the study period within 1 week after vaccination: 227 in the vaccine group and 91 in the placebo group. There was no statistical analysis of this difference, and no discussion of its possible influence on the "double-blind" design.
     In 2011, the Royal Society published "Experimental peripheral administration of oxytocin elevates a suite of cooperative behaviours in a wild social mammal.". The experiment was described as "double-blind", given the plan that neither the person who gave an injection to a meerkat, nor the observer of that meerkat's subsequent behaviour, would know whether the injection had contained oxytocin or saline. However, no evidence was adduced to show that this plan had worked (2729). Also see "...the introduction of new material".

          Research: grammar is an excellent guide to the substance of research studies.

     It is difficult to take a research study seriously when the author for correspondence declines to correspond at all (1073) (2640) (2856) (2860), or to completion (2800) (2802) (2812) (2863); see reference (2800) for a detailed example of the latter.
     When you assess a scientific experiment, ask yourself how hard the scientists tried not to find what they were looking for (R, pages 94-114) (351) (352) (353) (418) (444), and what they did when they found what they were not looking for (354) (1309) (928). A comparison of the abstracts of (499) and (500) is illustrative: both groups of scientists found a negative result, respectively no non-p5HT cell thermal responsiveness, and mean peak coherence of 0.018; the first group of scientists performed another, improvised experiment, and generated uneven positive results (499), while the second group of scientists explored the negative results.
     If A causes B, then attempts to explain C in terms of B should explore the relationship between A and C, for example, where A = trophic hormone, B = gonadal hormone, and C = neurogenesis (497). If A causes C and B may cause C, then the explanation of C in terms of B requires control of the relationship between A and C, for example, where A = the menstral cycle, B = leptin, and C = luteinizing hormone (802). The notional relationship between depression and bone loss requires the exploration of reduced mobility as a correlate of both depression and bone loss, and perhaps the use of hibernation as an experimental control (2432).
     Differences between human personalities requires the use of change scores within subjects (420) (1373), otherwise these differences may look like experimental effects between subjects. Repeated measures within subjects may lead to sampling artefacts (625) and to practice effects (562, Supporting Online Material, page 1), but these should be distributed randomly across the experimental groups. Repeated measures are certainly preferable, on theoretical grounds, to the assignment of one subject's score to another subject (562, Supporting Online Material, page 2), which meant that the experimenters made retrospective alterations to the experimental groups; this could have been avoided if all subjects had produced baseline scores, which had then been distributed randomly, and prospectively, across the experimental groups.
     Experimenters should use common sense, so that if someone is afraid of spiders, and is shown a picture of a spider and then a picture of a mushroom, it is hardly surprising that he or she is less aware of the picture of the spider than if he or she had not been shown the picture of the mushroom, because of distraction. It is an unwitting disclosure about the experimenters to call this "backward masking" and to consider that it "...excludes conscious processing of a stimulus..." (449), or that it enables "...the automatic processing of emotional stimuli without conscious awareness." (416). Consciousness varies over time, so that it is simplistic to divide mental life into either conscious or unconscious (2158). The subjects in this experiment may have formed a working memory of the picture of the spider, and may have been able to recall this on reflection, not least because of a nagging wish to explain having felt anxious about a picture of a mushroom. If a patient sample is aged between 16 and 48 months, then why assess it using the Social Communication Questionnaire, which is "...a 40-item yes/no questionnaire for children over 48 months."? (2654, page 561). Maternal sensitivity was assessed in two groups of children, one group in which the child had an older sibling diagnosed with autism spectrum disorder, and the other group in which the older sibling showed no signs of autism spectrum disorder, but maternal sensitivity was not compared between the two groups (2726). Meerkats were given injections of oxytocin in a carrier inclusive of chlorobutanol, and of saline, the injections being separated by three to five days, the authors concluding that the behavioural differences between the two injections were due to the oxytocin, which effectively said that if oxytocin = A, the carrier inclusive of chlorobutanol = B, and saline = C, then (A+B) - C = A (2729). See also "In 2011...". The Royal Society published a paper claiming that men with wide faces were more likely to perpetrate unethical behaviours than their female equivalents, without having controlled for the menstrual cycle in the experiment (2788): what was needed was a comparison between males and females, all with wide faces, and with the females all at the same ovulatory point in the menstrual cycle, at which point females are most likely to behave like males (2789). More differences at the nucleic acid level than at the protein level in human and chimpanzee genomes do not amount to differences between humans and chimpanzees, nor do explanations for those differences in terms of redundancies in the genetic code or differences in non-transcribed regions (2819, page 115). What is required is the demonstration of differences between humans and chimpanzees in differences at the nucleic acid level compared with the protein level, or of differences between humans and chimpanzees in redundancies in the genetic code, or in differences between humans and chimpanzees in non-transcribed regions.
     It is naive, at best, and disingenuously self-deceptive at worst, to suppose that respondents in a study are going to relinquish ideas that protect them from stress, especially when the design of the study does not offer other options (R, pages 220-221).
     Controls for psychological treatments are particularly difficult because of the immutable knowledge that a particular treatment is being given or not, and because of the network element, whereby the relationships between the researchers and the subjects generate changes (2337, pages 12-14): independent reviews are required after weeks, and again after months, inclusive of the family doctor and of involved relatives. Manipulation checks are essential (2557).
     The introspection of motor intentions has been shown to activate different brain areas than the introspection of motor actions (1155), which may be a study of the variable of introspection rather than a comparison of intentions and actions.
     Innovative measures such as "counterfactual thinking" (1629) (893), "counterfactual comparison" (1971), "fictive learning signals" (2049), "state" effects (1073), "valence" (1523) (1967) (1971) (2329), "valence-specific" (2016), "implicit and explicit conditioned valence" (2664), "salience" (2313), "clique percolation" (1923), memory ratings of "level of detail, emotion or personal significance" (1455), "drawing with significantly less regular velocity than controls" (2032), "repetition suppression" (1447) (2380) (2465) (2551), "the Lempel-Ziv complexity" (2438), "a modified version of the Sternberg paradigm" (2439), "fluid intelligence" (2441), "linguistic typological features" (2469), "modularity optimization" (2501), "rated masculinity or attractiveness" (2505), "attractiveness and masculinity scales" (2765), "odour preferences" (2532), "taster status" (2731), "trait dominance" (2533), "an index of facial masculinity" (2539), "male facial masculinity" (2663), "coyness" (2554), "biased attention" (2572), "evolved navigation theory" (2573), "judgement bias" (2576), "face and odour similarities" (2601), "dopamine tone"..."serotonin tone" (2622), "iconic visual memory" (2633) (2698), "facial cues associated with dominance" (2643), "self-resembling female nudes" (2661), "DNA content variation (DCV)" (2673), "fluctuating asymmetry and physical attractiveness"..."healthy and masculine appearance" (2686), "health ratings of raw male faces" (2706), "a suite of cooperative behaviours" (2729), "subliminally primed" (2736), "were rated for attractiveness by men, and were rated for dominance by both men and women." (2741), "Reward skewness coding in the insula independent of probability and loss." (2762), "neural signatures of evidence accumulation" (2763), "a robotic device to create patterns of facial skin deformation that would normally accompany speech production." (2777), "a bimanual robotic manipulandum" (2780), "affiliative behaviours during interactions with women." (2782), "avatar motion" (2786), "women's preferences for facial symmetry" (2790), "change of intention" (2794), "happy mimicry"..."angry mimicry"..."non-conscious mimicry" (2832), "individual intentionality (mentalizing) competences" (2814), "punishment"..."altruistic punishment"..."state-sponsored punishment" (2827), "both narrowband (NB) and broadband (BB) carriers (1/4- or 4-octave pink noise), which were jittered about a mean sinusoidal amplitude modulation rate of 0, 3, 29, or 57 Hz" (2857), and "startReact" (2908), require the accompaniments of test-retest reliability (2235) (2236) (2349) (2770) (2859) and of inter-rater reliability (2413) (2579) (2602) (2607) (2660), and then of validity (1246) (1026) (1301) (757) (1937) (2006) (2526) (2598) (2654) and (2859); indices of validity should be used to resolve contradictory findings (1279) (1796) (1816). Similar measures are required to actualise the difference between social responses and self-directed responses in primates (2206), self-reported life stress and rumination (1665), and fantasies that events of childhood can be elicited currently in young adults using telephone interviews and questionnares (943). The reliability and validity of what has been called "episodic memory" (2610) are tested on a daily basis when the witness takes the stand. Test-retest reliability is of particular importance with reference to the menstrual cycle, so that ratings of, and by, females are seen to be robust to hormonal variations: see references (2788) (2826) (2856) and (2802) as examples of the failure to do this, and see reference (2789) for details of human oestrus. Innovative techniques need to be compared with existent techniques (1335); (1341) (1654) (1693) (1970) (1989) (2363) (2616), especially if these have been based on illusions, such as parallax (R, page 237). Notionally new categories of disease, such as channelopathies (1602), need to be scrutinised carefully for an undue focus on similarities between diseases, compared with differences between diseases. Notionally new definitions require examples (2602, page 104). Claims of originality should be examined in the territory in which the claims are made (R, page 298), for example to ascertain the degree to which the claims are a challenge to the prevailing orthodoxy.
     Indices of reliability, that is agreement, need to allow for agreement by chance (3) (2602).
     Reproducibility, that is replicability (1684), using a technique that has been shown to be reliable and valid in the past, requires a thorough acknowledgment that both the performance of the equipment and the mental state of the intended user are potentially variable. A microscopist counting cells in the same part of the same slide with the same microscope on three successive days may produce an estimate of error (522), because the counts differ from each other and from the actual count, determined by consensus or by more advanced technology (1191) (1521). Potential error is added by the introduction of a second microscopist, and it is multiplied in the study of symptoms and signs of patients by a psychiatrist, because of the added variables of the psychiatrist's personality and background (3) (1931). Reduction of error requires any equipment to be calibrated immediately prior to use, by the intended user, against a criterion, such as a slide with a known cell count, or an interview format with agreed features, live or taped. Given the variables of personality and of background, it is sophomoric, at best, for psychiatrists to presume that calibration of a particular interview format at some point in the past, will endure or generalise (4) (5) (6). What matters is not the results of previous calibrations, it is the act of calibration, because this addresses the state of the equipment, and the mental state of its intended user, immediately prior to use.
     For an overview of diagnostic tests in psychiatry, see reference (2028).
     For an exploration of how clinicians diagnose what they expect to find, see reference (2374).
     For discussions of how experimenters find what they are looking for, see references (2433) (2430, page 27 and page 32) and (R, page 183, and page 200). Examples of this orchestration in psychiatry are the failure to consider that genetic changes may be effects rather than causes, the failure to study parents as much as their children, and the failure to use a control group with mental illness. If attempted disproof is the best way to reduce uncertainty (2167), then the failure to attempt disproof is consistent with a wish not to reduce uncertainty.
     A reliable and valid technique can be standardised across groups, for example, with respect to age (1681) (1636).
     The results of an experiment may reflect the fact that subjects were given information that might not have been true (468) (981), or that was untrue (2927).
     Studies over a few days of students by their teachers may not generalise, especially if the students have been misled by the teachers (507) (508) (2514).
     Any experimental design that requires the subjects to be misled needs to be seen to be tested as to its success after the experiment, thereby to allow the results to be interpreted in an ambience devoid of experimenter omnipotence. The act of having misled the subjects needs to be seen to be discussed as part of the debrief after the experiment.
     Any experimental design that entails an artificial game requires information about how the subjects were recruited, what the subjects were told they would be doing, what rewards the subjects were given, whether the subjects were debriefed by the experimenters, and whether the experimenters were debriefed by the subjects.
     Researchers who use their students as experimental subjects may produce results that reflect the students' responses to their teachers (2514).
     Only limited conclusions can be drawn from studies of the disembodied, for example, a hand viewed from above (548), and a rubber hand (2045); of the reconfigured, such as rats with trimmed whiskers (696); and of the unrealistic, such as repeated vowel sounds (549), nonwords (345), non-words (511), digital organisms (753), overlearned arbitrary visuomotor associations (1089), semantically unrelated word pairs (1294), unrelated word pairs (2027), and pseudowords (1416) (1952).
     Results may be influenced by the investigation itself, called the Hawthorne effect, named after the Western Electric company plant, where it was first observed (665) (R, pages 152-159); (1155) (1932) (2672).
     Results may reflect the design of the experiment, such as the populations sampled (2124), the sampling frequency (2008), and the failure to use a control group with mental illness: see references (2467) (2483) and (2589), and compare references (765) (766) (1699) (1770) (2012) (1799) (1869) (2208) (2277) (2371) and (2447) with references (756) and (2438). Face preferences may reflect gender preferences (1813).
     Contradictory results may reflect differences between patients and normal subjects (1227).
     Results may reflect medication (742) (782) (765) (743) (766) (1699) (1770) (1799) (1869) (2208) (2371) (2438) (2483) (2547).
     Results of experiments may not generalise (964) (1066) (894), because the sample was too small (924) (1020) (2061) (2640) (2898), because of observer effort (2707), because the cerebral cortex was studied in isolation (1053) (1420) (1910), because the amygdalae were accessed through the eyes in one study (1545) and through the visual fields in another study (1546), because of differences between species (2749), between genera (2485) (2767), between families (1806) (2767) (2749), between orders (1085) (1806) (1075) (1138) (1206) (2038) and between classes (2560) (2851), because of the effects of captivity (600) (677) (693) (2289) (2328) (2749), of anaesthetics (99) (954) (1483) (601) (1139) (1235) (634) (658) (991) (1421) (1753) (2279) (2299) (2456) (2466) (2649), of different types of lesion (1549), of temperature (1366) (1531) (2646), of post-mortem changes (2549), of the position of an electrode, both stimulating (1562) and recording (1744), of the frequency, intensity and duration of stimuli (2749), and, relatedly, because of the very wide range of stimuli, such as 80 microA (900), vibration at 83 Hz to produce the illusion of movement (1015), bipolar electrical stimuli (2071), high-frequency stimulation (1452), low-frequency stimulation (1809) (1857), microstimulation (2004), subthreshold microstimulation (2044), electrical microstimulation (2445), stimulation at pulse frequencies ranging from 50 to 300 Hz in anaesthetised, ovariectomised rats (2241), transcranial magnetic stimulation (2354) (2402) (2448) (2769) (2792) (2821) (2823) (2871) (2875) (2879); (197) (547) (1386) (2222) (1960) (2021) (2123) (2347) (2543) (2632) (2779) (2825) (2831) (2850) (2925), repetitive transcranial magnetic stimulation (541) (2322) (2730), fast repetitive transcranial magnetic stimulation (2097), low frequency repetitive transcranial magnetic stimulation (2325) (2081), subthreshold 5-Hz repetitive transcranial magnetic stimulation (2893), transcranial magnetic stimulation in different directions (2711), transcranial magnetic stimulation at suprathreshold strength (2894), theta-burst magnetic stimulation (2565), theta-burst stimulation (2665) (2689), subthreshold transcranial magnetic stimulation (547), a subthreshold transcranial magnetic stimulation pulse (1963), single-pulse transcranial magnetic stimulation (2621), double-pulse transcranial magnetic stimulation (2652), paired-pulse transcranial magnetic stimulation (2119), triple-pulse transcranial magnetic stimulation (2642), focal transcranial magnetic stimulation (2603), transcranial direct current stimulation (1954) (2064) (2690) (2768), anodal transcranial direct current stimulation (2732), cathodal transcranial direct current stimulation (2732), repeated transcranial direct current stimulation (2716), slow oscillatory and constant anodal transcranial direct current stimulation (2621), unilateral and bilateral transcranial direct current stimulation (2866), paired-associative stimulation (2891), transcutaneous electrical stimulation (2497), a pin-prick in the cerebral cortex (1604), artificial whisking at 5 Hz in anaesthetised rats (1613), morphing (1886) (1892), a continuous 3D morph (2359), and a fake snake (918). Results of studies of the interaction between genes and the environment may not generalise, because of the differences between the environment defined in terms of its physical characteristics, and the environment defined in terms of the people in it, which caveat applies particularly to simulation models (2341, page 586).
     Anterograde anatomical tracers may also be transported retrogradely (877). Hodological standardisation (1357) and validation (1937) have been attempted.
     Results of studies of the in vitro slice may differ from results of studies of the organotypic culture, and both may differ from results of vivo studies (1486) (1374).
     Readers should be wary of scoring that was double-blind when the subjects were fish (1908), of results that were analysed in a double-blind fashion when the subjects were mice (461), of the statement that investigators were blinded to the treatment group in a histological comparison of wild type and D1 null mice (873), of the inability to replicate a study due to a lack of clinical criteria (467), and of the citation of "depressive-like traits" as "schizophrenia related phenotypes" (2239).
     The anthropomorphic assumption that adult human attributes apply to animals, (R, pages 18-25) (459) (465) (552) (1158) (2098, page 191) (2151) (2212) (2218) (2278) (2411) (2580) (2729) (2863), to infants (637) (2190) (2116), to children (R, pages 206-219) (2117) (2267), to parts of the body (2153), and to neurones (2306), requires circumspection, as does the anthropomorphic ascription of human stresses to genes (716) (718) (475) (720) (875), of human activities such as "house-keeping" to genes (2617, page 96), and of "deep genetic homologies" that conspire with the discovery of fossils to offer fresh insights (2889, page 820). Animals can condition humans (R, page 66, page 123, and page 139) (2098, page 191).
     Responses may be counted, or they may be measured, so that it is not meaningful to refer to a mean of 10.2 items (2514, page 121), and to 7.8 recordings, 229.5 conversations and 226.2 monologues (2654, pages 559 and 565): the mode or the median should be used. Similar reservations apply to the ubiquitous, but nonetheless questionable, practice of applying numbers, such as 1, 0.5, and 0, to each of a set of responses, such as "agree", "unsure", and "disagree", and then processing the set of responses as a scale that has the same equal intervals between each of the responses as have the numbers (2602, page 105), not just within one respondent on one occasion, but also within one respondent across occasions, and between respondents: the degree to which we agree relative to being unsure may be different from the degree to which we disagree relative to being unsure; the presumption of equal intervals enables the use of parametric statistics (2654), which assume equal intervals, but it disables the variety of life, and it reduces the variance of samples of responses through the elimination of extreme responses, so that any two such samples are less likely to overlap and are thus more likely to appear to come from different populations, when, in fact, they come from the same population; the more realistic, less opportunistic procedure is to process the responses as categories or as ranks and to use statistics that do not assume equal intervals, and that, therefore, do not make the real response: "I agree very strongly indeed." appear to be of the same degree as the real response: "I disagree.".
     The use of large samples does not reduce error if the study variable changes over time and if samples are not taken from each time period. Taking the mean of such a large sample without reference to time period results in a loss of information (2802). If a study variable changes above or below baseline over time, then sampling without respect to time results in a dilution effect. If a study variable changes both above and below baseline over time, then sampling without respect to time results in a negation effect.
     The probability of falsely rejecting the null hypothesis, called the alpha probability of the type I error, and the probability of falsely accepting the null hypothesis, called the beta probability of the type II error, can be estimated before an experiment is implemented. Missing something that is really present, that is a false negative and a function of sensitivity and of type II error, has to be balanced against finding something that is not really present, that is a false positive and a function of specificity, and of type I error (457), for a given sample size (572). Thus, an increase in sensitivity, that is a reduction in false negatives, may result in a loss of specificity, that is an increase in false positives (1070) (1678). Sensitivity and specificity are indices of validity. The identification of true negatives requires a context and a duration of observation adequate for a spontaneous response to occur (2098) (2206). Statistical significance is measured in degrees, so that it is arbitrary to gloss over a more significant result, and explore one that is less significant (552). The more statistical tests that are performed on a set of results, then the more likely it is that some of those tests will be significant by chance, and this should be acknowledged in the results (2602, page 107). Raw data should be published to allow critical evaluation (2144), so that every scientist is able to perform an analysis incorporating his or her preconceived models (566).
     Repeated measures of the same subject are not the same as separate measures of different subjects, and they require different statistical tests, which compare the differences between repeated measures with no difference, that is 0 (2640).
     Publication bias has been addressed in reference (2191), and experimental bias has been addressed in reference (2842).
     Correlations are not causes (1453) (1281) (1444) (1630) (1798) (2399) (1953) (2207) (2508) (2606) (2679).
     Correlations in the present may reflect relatedness in the past (2766).
     Effects may be causes of the notional causes (2145) (1955) (2105) (2092) (2419) (2491) (2601) (2637, page 119).
     Reference (269) is an exemplar of technical (407) (408) and statistical (409) standards.
     The presentation of a scientific report is instructive: the writer's wishes are conveyed by heavy type (2791), upper case, italics (R, pages 35-59) (1875) (2267) (2564, page 3054) (2697) (2726) (2798, page 129, patterns) (2854) (2888, deep homology), underlining, and hyphenation (2431) (247) (2889) (2892) (2900) (2923), while the writer's doubts are conveyed by brackets (2416) (2814) (2900), and by quotation marks, such as "phase precession" (629), "double-blind" (630), "whisker pairing" (694) (695), "deactivations" (769), "overeating" (807), "normalizes" (856), "abstemious"..."greedy" (875), "dual-match stimuli"..."release" (885), "pragmatic relevance" (967), "cue recruitment" (1136), "standard model" (1137), "liking" (1159), "cochlear amplifier" (1233), "amplify" (1896), "plastic" (1353), "grid cells" (1396), "moire grids" (1899), "remapping" (1434), "partial remapping" (1476), "rate remapping" (1874), "global remapping" (1874), "impartial" (1440), "repetition suppression" (1447), "cell assembly" (1477), "memory fields" (1492), "tag" (1495), "feedforward" (1502), "general arousal" (1565), "replay" (1566), "positive illusions" (1576), "mirror" (1785), "action-listening" (1797), "fearful"..."disgusted" (1892), "schema" (1928), "microcircuit" (1933), "zoom lens"..."multiple spotlights" (1939), "hyperdirect" (1951), "disorder,"..."order," (2022), "windows" (2034), "mood stabilizer" (2035), "superorganism continuum" (2046), "warm glow" (2094), "noninformative vision" (2121), "resting" (2131), "disappear" (2146), "external monitoring" (2147), "fractals" (2156), "higher-level" (2209), "action-constrained" (2232), "audiogenic"..."rate maps" (2240), "noise" (2251), "real-life" (2266), "alert" (2308), "altruistic" (2330), "trade-off"..."having it all" (2342), "geometric module"..."cognitive map"..."declarative"..."episodic"..."procedural"..."bottom-up"..."top-down" (2416), "small-world" (2381), "effects" (2384), "intuitive statisticians" (2393), "selfish punisher"..."pay" (2440), "fingerprints" (2484), "memory" (2522), "sexy daughters"..."sexy sons"..."good genes"..."correlated response theory" (2536), "winning"..."losing" (2539), "gate opening" (2542), "anxiety-like" (2546), "limping behind"..."caused"..."catch" (2547. Comment.), "catcher" (2813), "social awareness" (2574), "cooperative" (2575), "on-demand" (2593), "strangers" (2615), "Instinct to Teach" (2624), "emotionally negative" (2664), "DNA content variation (DCV)" (2673), "eye-field" (2698), "genetic asynchrony" (2705), "binding" (2718), "supernatural watcher"..."behavioural priming" (2736), "spiteful" (2737), "social affiliation" (2606), "mistakes" (2764), "global suppression"..."anticipation phase"..."stopping" (2779), "curved"..."sensory selection" (2780), "automatic" (2785), "channels"..."preferred" (2787), "pitch center" (2791), "glandular" (2798, page 131, footnote 3), "gets it wrong" (2803), "duplicated processing"..."low level"..."deep" (2807),"code of honour" (2852), "default mode network"..."executive control network" (2868), "deviant"..."primitive intelligence" (2869), "teaching occurs but is rare"..."retarded" (2884), "break"..."near-neutral"..."mosaic" (2885), "program"..."paddle" (2889), "tactical level" (2897), "mer
eological fallacy"..."largely descriptive"..."evo-devo"..."mesoscopic scale"..."grid-based"..."big data"..."functional"..."understanding"..."function"..."reference"..."blind men and the elephant"..."pan-optic neuroanatomy" (2900), "sculpting the response space"..."insight" (312), "choice option" (2921), and "abnormal" (2930). The combination of brackets and quotation marks emphasises the doubts (2418) (2858) (2892) (2902).
     The use of the present tense in the description of experimental results reflects the fantasy that what actually happened in the past tense of the experiment, generalises: see the abstracts of references (124) (431) (432) (433) (434) (435) (1807) (436) (1610) (1780) (1830) (1842) (1955) (2065) (1883) (2005) (2210) (2232) (2372) (2504) (2510) (2569) (2578) (2636) (2664) (2725) (2729) (2757) (2774) (2815) (2816) (2827) (2832) (2855) and (2886). Especially revealing are changes between the past tense and the present tense during the description of results, as in the abstracts of references (124) (435) (1119) (456) (460) (464) (1454) (1526) (466) (533) (534) (874) (951) (1612) (1679) (1772) (1787) (1791) (1810) (1946) (2053) (2054) (1895) (1938) (2119) (2209) (2219) (2233) (2264) (2265) (2304) (2311) (2314) (2315) (2320) (2336) (2394) (2419) (2431) (2483) (2489) (2492) (2507) (2543) (2555) (2561) (2587) (2632) (2643) (2719) (2734) (2739) (2741) (2758) (2759) (2767) (2825) (2826) (2830) (2857) (2874) (2883) and (2909). To some degree, the results of an experiment may reflect the format of that experiment, which is for the reader to decide (R, page 299), and is certainly not for the experimenter to discount. Insofar as generalisation is warranted, the verbal mood should be subjunctive or conditional, as distinct from indicative or imperative.
     Figures of speech raise doubts. For example, the use of metaphor suggests a cognitive switch, possibly toggle (800) possibly flip-flop (813), and a lack of penetration of thought (2484) (2637) (2602, page 107) (2666) (2783) (2889) (2900) (2906). Ellipsis of language suggests ellipsis of thought (897) (1088) (727) (2223) (2707), and has been associated with what appears to be excitement (1515). Oxymoron portends ambiguity, for example "statistical instabilities" (1898), "fixational eye movements" (2089), "The 'Instinct to Teach' " (2624), the somewhat impenetrable and circular concept of "voluntary spontaneous motor acts" (1157), and the defiantly inaccessible "non-mnemonic role of the prefrontal cortex,...monitoring...information held in memory." (521). Personification anthropomorphises, and thus obfuscates (1650) (1714) (2885). It is all too easy to personify mental processes, for example, those that conspire (639). Hyperbole defines personal limitations (1602) (718) (1851) (2431) (2885) (2889). Puns may disclose fantasies, the moreso if in quotation marks (1894). The use of eponyms is narcissistic (2438) (2439), and leaves the reader with much to unravel, as in the distinction between non-Duchenne and Duchenne laughter (1906) (286) (565) (2796), which is much less accessible than the distinction between movement of the lower face only, and movement of both the lower face and the upper face, during laughter: connotations of the distinction can then be expressed in terms of identifiable muscle groups, and, more to the point, in terms of their nerve supplies, rather than in the name of a neurologist who published in 1862 (1907): references (2323) and (2324) illustrate the disarray that can follow the use of eponyms: reference (2352) shows the inconsistency indicative of ambivalence about eponyms, suggestive of insight. The offensive metonym "schizophrenics" is Inadvertent Social Information about the speaker (2519), who can then be placed squarely in a biological context (589) (666). Euphemism conveys that there is less to the statement than meets the eye (2729) (2885) (2895).
     Uncommon words, and uncommon combinations of common words, suggest a lack of insight into the evolution of jargon by people who work closely together, for example, "deconfound" (416), "a confound" (456), "deconvolve" (2340), "desuppression" (437),"counterregulatory" (462), "repressilator" (843), "affordances" (1825) (2856), "subchronic" (1883), "manipulandum" (1960), "suicidality" (2030), "phenogenetic" (2043), "pseudoarithmetic" (2106), "nonkin" (317), "nonconscious" (2237), "non-conscious" (2832), "nonconsciously" (2919), "mentalize" (299) (638), "speciose" (2341), "unisensory" (2431), "ecocultural" (2491), "aggressees" (2506), "nonpainful" (2528), "disassortative" (2532), "nonprogressive" (2547. Comment.), "numerosity" (2060) (2178) (2592), "nonaction" (2569), "aspecific" (2793), "nonidentified" (2826), "deep tree-like pattern" (2381), "non-primary" (1242), "nonprimary" (2857), "populational" (2884), "relitigate" (2885), "nonhomology" (2888), "non-model" (2889), "datasets" (2900), "nonhuman" (2915), and "distractive" (1302). Quotation marks around an uncommon word, such as "hyperdirect" (1951), "nonallocation" (2146), and "featural" (2494) suggest insight into the evolution of jargon by people who work closely together, as do quotation marks around uncommon combinations of common words such as "ideal reacher" (2120), "dual-language" (2159), "non-mirror transformation" (2370), "interaction environment" (2538), "judgement bias" (2576), "mesopontine rostromedial tegmental nucleus" (2560), "sequence rule"..."probability rule" (2613), "sexually antagonistic zygotic drive (SA-zygotic drive) of the sex chromosomes"..."no-cost-to-self nepotism rule" (2669), "two-armed bandit" (2740), "formant position"..."formant dispersion" (2784), and "mesoscopic scale" (2900). The appearance of quotation marks around words within a text suggests that doubts have occurred as the author has been writing, for example "mosaic" (2885, second and sixth paragraphs), and "vertebrate-type" (2889, reference 12). The disappearance of quotation marks from words within a text suggests that those words have been integrated into the language as one has been reading, for example, "modularity" (821), "set" (892), "aperture problem" (2103), "utilitarian" (1986), "irrational" (1836), "ghost" (2345), "accumulator" (2648), "SA-zygotic drive" (2669), "automatic imitation" (2785), "channels" (2787), "catcher" (2813), "slowing down" (2837), "quality" (2840), "intrinsic chance" (2854), "altruistic punishment" (2827), "attentional effort" (2874), "disembodiment effect" (2883), and "reverse colinearity"..."phase 2 expression" (2889), and "functional" (2900). It is contradictory to invent the word "disfluent" to describe findings in a study of preferred fluency (914), to invent the word "dispreferred" in a study of language universals (2496), and to consider an interpretation that relies on "reverse inference" (1778). The use of words from another language, is, at best, convoluted, and is likely to lack the precision of one's own language, with its own distinctive set of rules (1779); (377) (2039). A change in language conveys uncertainty, the moreso the more rapid the change: thus one researcher referred to his list of items as "a diagnostic instrument", "the test", and "the test instrument" within the same paragraph, which variation was compounded by the researcher's reference, within the same paragraph, to "test results", which were not, in fact, results produced by the list of items, but were the results of a validation of the list of items, which were therefore notionally independent of the list of items and thus of any results produced by the list of items construed as a test (2514, page 121). Abbreviations such as "etc." abbreviate the reader's focus (2281).
     Prodigies of scientific endeavour are undermined by spelling errors, as in "pubic health surveillance." (493), "discreet regions of the brain," (1515), and "more than one compliment of C57BL/6 and 129/S1 alleles" (2618), by the use of superlatives to describe comparisons, for example, between the sexes, which must, perforce, be more than two in number (1759), by a switch from the past tense to the present tense in the description of the results of a study of perceptual switch rates in bipolar disorder (2483), by the use of a singular noun with a plural verb (2312), by the use of a plural noun with a singular verb (2458) (2515) (2885), by the use of a plural subject with a singular verb (2900), by the failure of the author of a report about "episodic memory" to remember to include all his references (2610), by the omission of a reference in an article about lifestyles and cognition (2707), by a sentence without a verb in a text about lost copies (2617), by the use of the word "arsenal" to describe tools used in social environmental contributions to autism (2654, page 568), by a figure that describes monotremes as metatheria and marsupials as prototheria in contradiction of the text (2748, page 10, Fig.1), by the uses of the words "varying" (2853), and "variable" (2749), which mean variation over time, instead of the words "varied" or "different", which mean variation at one point in time, by familiarity (2889), the moreso if the familiarity is inconsistent (2900), and by value judgements, particularly in a study about value (2921).
     The content of an abstract should reflect its title (561) (1876) (1888) (2339) (2630) (2788) and should make sense (526) (1120) (756) (1537) (1644a) (1088) (897) (1317) (1526) (909) (949) (2000) (2069) (2096) (2241) (2411) (2833). The content of an article should reflect its title (2637) (2788) (2819). Language should be consistent (939) (2352) (2707) (2708). Conclusions may extend beyond results (2113) (2020) (2159). Self-centred mental imagery need not require neuroimages; it may be evident from the authors' opinion of their own work as useful (869). The introduction of new material towards the end of an abstract should raise concerns. For example, reference (2109) is entitled: "Male twins reduce fitness of female co-twins in humans.". The abstract is clear and coherent until the last sentence, wherein the term "adaptive sex allocation" is introduced. Recourse to the full text reveals that the word "allocation" is not used until the last paragraph of the discussion ("Finally...", page 10919), within the term "optimal sex allocation", and that the term "adaptive sex allocation" appears only in the abstract and thus is not discussed. In addition, the terms "sex-ratio" and "sex ratio" are used in the same paragraph ("Finally...", page 10919), without explanation as to any differences between them, and the term "sex ratio" is specified as "litter sex ratios" ("Therefore...", page 10915), "gestation sex ratios" ("Finally...", page 10919), and "maternal sex ratio" ("Finally...", page 10919), again without explanation as to any differences between these terms. There inconsistencies hint at an uneasy relationship between authors, referees, and editors, and at a corporate failure to appreciate the degree to which loose language undermines clarity of thought. Again, in reference (2700), some of the findings are explained in the penultimate sentence by the introduction of the idea that activation in the subcortex is less potently modulated by attentional state. Rather than speculate outside their own findings, the authors should use that sentence to tell us about the interaction between tinnitus and hyperacusis in their subjects, and the referees and editors should see that they do. A melodramatic variant is when the object of a study becomes the subject of that study (2717).
     Concerns are evoked by the introduction of new references as a paper progresses through the results and the discussion (247), and by the introduction of new material in the legend to a figure in the results (2729). See also "...a suite of cooperative behaviours...".
     Claims of originality require the utmost care, and if in doubt, the subjunctive mood and the conditional mood are preferable to the indicative mood (1558).

     Attribution of mental states to others requires an evidentiary basis to dispel the suspicion that the attributors are really talking about themselves (2884).

          Prevention: mental health is the absence of mental illness.

     In England, mental illness is allowed to develop, and is then managed using unreliable diagnoses and inadequately researched treatments. There is no workable description of mental health, so that the prevention of mental illness is well nigh impossible. How can one identify the deterioration from something that is not described into something that is described loosely? Parents and teachers need something against which to test their instincts (1656).

     Mental health may be defined as the capacity to review independently one's mental state as it is perceived by others. Mental health is facilitated if one is able to see oneself through the eyes of other people and to hear oneself through the ears of other people, as judged by their responses, within one's habitat and within one's territory. Developmentally, is a child learning the potential difference between the "I" in "I see you." and the "me" in "I see you seeing me."? [Back to selection if required.]

     The evidence from evolution is that we begin life with the potential for these capacities (1220) (16) (14) (15) (811) (719) (2194) (2250). The evidence from over 80,000 consultations in a psychiatric consultancy of 25 years, is that this potential can be undermined by events within the habitat (17), specifically loss of instincts due to fear, with consequent schizophrenia, and failure to achieve independence, with consequent depression and mania.

     A more detailed appreciation of mental health can be gained through the remainder of this text, which describes the structure and function of the healthy brain, relates this to stress, and then explains how what is called "mental illness" can arise out of these structures and functions when the habitat and the territory are unfavourable, and how this developmental calamity can be avoided.

     We inherit through our genes an array of potential responses, but these require to be developed for us by our family (2129), even if they do not use those responses themselves. If the responses are developed, then we are able to reduce our unfitness through cooperation in Society.

     Our genes limit our instincts. Our genes limit our potential to inhibit our instincts. Our genes do not limit the potential of the adults who rear us to influence our instincts and our potential to inhibit our instincts. Hence the limited predictive value of genes in relation to mental illness (860) (1929) (1930).

     There is a major difference between an adult who does not learn to become independent within his or her habitat, and who carries that lack of capacity into his or her territory, and an adult who does learn to become independent within his or her habitat, and who brings that capacity into his or her territory (342). Such a difference may have hierarchical and clinical consequences (973) (1324). Habits learned in the habitat may not be acceptable in the territory (R, page 271).
     An appearance of mental health may be achieved through affiliation with like-minded people, but this may not generalise.
     For humans, the habitat and the territory are represented by memories in the cerebral cortex, and these representations include memories of other people. At any moment, a change in feeling, mood or emotion, prompts the human to locate the explanation for that change in its representations of itself, of its habitat, and of its territory, and thus in its representations of other people. Enactment may follow, as in: "Look what you made me do." Emotional abuse of children occurs when adult humans locate the explanations for their own moods inside those children. Parents have to inhibit their own predatory instincts if they want their young to develop (2625). Adult human relationships may be adaptive because they extend explanatory space into the real habitat and the real territory. The ability to see and hear oneself through other people in one's habitat does not necessarily imply the same ability in one's territory, and vice versa. In the brain of the occupant, neuroanatomical differences between the habitat and the territory include the distribution of visceral activity, while endocrine differences include the distribution of oestrogen and progesterone (2358), chorionic gonadotrophin, oxytocin, and prolactin (2346) (2356).

     One may choose not to use the capacity to review independently one's mental state as is it perceived by others, which is an expression of one's personality. One may discount some or all of the results of an independent review of one's mental state as it is perceived by others, which may reflect any of one's personality, a judgement about the others, and force of circumstances; one's personality the moreso if the discount is habitual, and thus independent of which others and of which circumstances. The capacity to review independently one's mental state as is it perceived by others increases with imagination and decreases with fatigue, with physical illness and with age. The lack of the capacity to review independently one's mental state as it is perceived by others does not necessarily mean that one is mentally ill in the conventional sense, it means that one is not mentally healthy, in the physiological sense that one lacks homeostatic capacity and in the social sense that one is not capable of independence, at the time in question.

     An animal that sees itself through the eyes of its predator and hears itself through the ears of its predator increases its chances of survival (451) (1023) (1072) (1767) (2048) (2472), as does an animal that sees and hears itself through the eyes and ears of its prey (1295), and as does an animal that sees and hears itself through the eyes and ears of conspecifics (1104) (2162); (1438); (1105) (1666); (2257) (1768) (1823) (2217) (2270) (2609) (2805) (2896) (2897), including mates (1106) (1999), and thieves (1299) (1363), especially if the animal has the instinct that it may not be seen and heard accurately (280) (1103). Effectively, the animal's cerebral cortex contains visual and auditory representations of itself and of other animals, which representations may include memories. Separate nerve circuits may exist to locate other animals (1769), and to locate oneself through other animals (1729) (2095) (2493). If a bigger brain means more brain cells (1887), then it may confer an advantage: all the better to see you through your eyes and to hear you through your ears. Ritual fights provide practice (18) (1559) (610) (685) (1107) (2204) (2344). Generosity may improve partner choice (423). If habitat and territory are seen as reproductive space, then any reduction of fertility due to mental illness, or to its treatment, can be construed as altruism (702), allopatry notwithstanding (710). For a discussion of the operational definitions of habitat and territory, see reference (751), and for a discussion of the problems of ecological units, see reference (1683). For indications of the importance of reproduction in the interplay between selfishness and selflessness, see references (812) and (817). For the exploration of genetic nepotism, see reference (1270). For a proposed mathematical solution, see reference (819), but bear in mind that the underlying theory characterises real people as either cooperators or defectors (474) (985), when, in fact, they can be both (2440); at the same time in the habitat, as in the ambivalence of passive aggression, and at different times in the territory (2130), as in share dealing. Figure two configures some of the variables that require consideration.

Figure two

     It is helpful to reflect on possible differences between doing nothing, and not doing something.

     Adaptive responses such as homeostasis, phenotypic modification and phenotypic plasticity, however defined (2341) (2535), are likely to entail both the inhibition of responses that are now maladaptive and the activation of responses that are now adaptive, and the rates at which these two types of responses are produced need not be the same, due to their intrinsic chemistry. For example, there may be a temporal difference between the synaptic inhibition outside a cell of a chemical released by that cell through the sequence nuclear DNA, cytoplasmic RNA, and cytoplasmic protein, and the inhibition within that cell of the sequence nuclear DNA, cytoplasmic RNA, and cytoplasmic protein so that the aforementioned chemical is not released into the synapse in the first place. It follows that the rate of environmental change may be selective, and that, insofar as humans can alter the rate of environmental change, then they can be selective of one another, as in timed targets. Relatedly, an adaptation that is required due to a change in place may be easier to implement than the same adaptation due to a change in the environment in the same place, because of the time necessary for travel.
     Insofar as adaptations entail the inhibition of responses, which responses have a genetic component, that is to say they have been derived to a degree from the genotype of twenty-two pairs of autosomes and one pair of sex chromosomes in each cell, then adaptation entails inhibition of genes, referred to hereafter as genetic inhibition. It is likely that inhibition itself has a genetic element, so that genes inhibit genes, included in the genetic concepts of epistasis (735) (788) (1642) (2753) and hypostasis. Genetic inhibition may be one of the functions of the DNA that does not code for protein (2607) (2798) (2819) (2858).
     The reconfiguration of genes that occurs during meiosis may be explicable as disinhibitory, so that the genes inhibited through force of circumstance in the parent are reactivated and made available in uninhibited form for the next generation.
     The seemingly suicidal behaviour of lemmings (1112) and of red grouse (D) becomes less inaccessible through the derivative concept of a hybrid, part inhibited and part activated: fight is inhibited, so flight ensues. We are able to review as incomplete, erstwhile concepts of group selection (1113) (1114) (1115) (1116) (1912) and kin selection (1112) (1113) (1117), because they are so focused teleologically on genetic activation in the future (2088), that they fail to address genetic inhibition in the present, and so are made to appear separate processes, when they are, in fact, two aspects of the same process (1948) (1949): that is, survival of the less unfit through cooperation, irrespective of relatedness.
     Childhood may require phenotypic modifications that are inhibitory of the child's genotype, and to the degree that the genotype becomes irretrievable, mental illness looms. In biochemical terms, what happens to the nuclear DNA, cytoplasmic RNA, and cytoplasmic proteins that produce a neurotransmittter, if the release of that neurotransmitter is inhibited consistently during formative years?
     There is a major difference between a family wherein the offspring are cultivated in their own right, that is independent of adult activities, and a family wherein the offspring are part of a division of labour inclusive of adult activities, because the distribution of responses in a division of labour necessitates genetic inhibition, that is the inhibiton of genes that produce the responses to be delivered by the other parties, and genetic activation, that is the activation of genes that produce the responses to be delivered by oneself. Each inhibition and activation is likely to have chemical and hormonal consequences, with obligate chemical time constants necessary for the inhibitions and activations to be constructed at a molecular level.
     One of the chemical consequences of inhibition and activation is the
expenditure of chemical energy, so that these processes are costly, and this is one of the confounding variables of formal intelligence tests. The more chemical energy that a child has to expend on the orchestration of responses that enable survival in the family habitat, then the less chemical energy the child has for cognitive activity.
     Genetic inhibition is subject to hormonal influences. Males get so detached from parts of themselves that they are unable to access those parts introspectively, and can only do so through their senses, in sexual activity.
     Alcohol is used to disinhibit otherwise concealed genes, with less ownership of the denouement than would occur in sobriety.
     The concept of sexual equality has encouraged women to discount real differences between themselves and men (1588), which has exposed an entire generation of women to lack of preparedness for middle age, to the degree that some lives have been shortened. One form of suicide is the corporeal ending of a life that is dead already.
     The more we inhibit ourselves, and thus our genes, then the more likely we are to experience that inhibited part of ourselves through our senses, that is, to see and hear ourselves as another person through our own eyes and ears. The inhibition is of subcortical activity by cortical activity, which exaggerates the degree to which our responses to external stimuli appear to come from those stimuli rather than from ourselves, so that we experience paranoid misperceptions. What is actually an apperception is experienced as a perception. There is a reduction of the corollary discharge that normally signals ownership.
     The more that a human is inhibited by another human, then the more likely he or she is to experience that inhibited part through the senses, as another human: the more that a human inhibits himself or herself, then the more likely he or she is to experience that inhibited part through the senses, as another human: adult humans do not often inhibit themselves unknowingly because other adult humans inhibit them, but children do, with the consequence of mental illness.
     An organism cannot see and hear itself through the eyes and ears of other organisms if there is no self to see and hear, because of the formative inhibition of instinctive spontaneity by other organisms, and then because of the learned inhibition of the organism, by the organism itself (P, page 300).
     The concept of genetic inhibition can be applied to theories of language (2185) (2155) (2333), which need to explain why there is a lack of distinction between subjects and objects in the language of some adult humans some of the time, as in the regressive: "Look what you made me do.", which statement emphasises the reducibility of language. Actually, the syntactic subject "I" exists at two levels; a primitive subject which perceives objects (2509), and a cultivated subject which perceives objects perceive itself, the subject, as it experiences itself introspectively through its instincts: "I see you." and "I see you seeing me." respectively. Given the subject's capacity to perceive objects, and given that the subject has introspective capacity, the degree to which the object mirrors the subject (2098) as the subject experiences itself introspectively becomes the crucial variable. To what degree is the subject genetically inhibited and genetically activated in the presence of the object? Verbal learning of syntactic rules (2257) at school, without the experience of being perceived in one's own terms at home, is duly expressed by the primitive "I" as the uncultivated mixture of subjects and objects found in hallucinations and delusions, when the adolescent starts to speak for himself or for herself: "I can hear the instructor talking about my driving.". Syntactic rules are not determinate, as evidenced by the fact that many patients with hallucinations and delusions use syntactic rules accurately to describe working relationships with people about whom they do not have hallucinations and delusions. The syntactic subject is formed out of the syntactic object, who conveys, partly through syntactic rules, that the subject exists outside the object. The syntactic subject sees and hears itself through the responses of syntactic object. What is determinate, then, is the perception by the subject through his or her eyes or ears or both, of responses that reflect his or her introspected instincts, which responses may then be described through syntactic rules. An implication for clinical psychiatry is that when a child or an adolescent is troubled, then neuroimages are required of all the members of the habitat, and not just of the notional "patient". An issue for university psychiatry is the usefulness of empiricism, where that means verbal responses within which introspectively accessible meanings have been ignored, for example, through a lack of formal attention to vocalisation (2838): the "Yes" that means "No", and the "No" that means "Yes". For a more detailed, cellular illustration, see Brain cells.

A QUICK GUIDE TO THE DEVELOPMENT OF MENTAL ILLNESS.

     The brain has an engine (e), capacitors (c), a distributor (ds), gears (g), a steering wheel (sw), a driver (d), brakes (b), a seat for a driving instructor (di) and a map of the world (mw).

Figure three

     During early life, the driver is guided by a driving instructor, who lets the driver take charge at times. The driver learns how to drive safely, with consideration for others but with allowance for careless and dangerous driving by others. The driver learns maps of the world, and also what to do if lost and if there is a breakdown. After fifteen years, the driving instructor withdraws gradually.

     The essence of what has been called "schizophrenia" is that the driver is afraid of the driving instructor or of the world or of both, so that the driver lets the driving instructor do all the driving. The driver may pretend to explore the world under the guidance of the driving instructor, but really, the driver is only going where he or she thinks the driving instructor wants him or her to go. Consequently, when the driving instructor leaves, the driver is unsafe, inconsiderate, naive and headstrong, and attempts to explore the world bring to mind memories of the driving instructor, as in: "I can hear the instructor talking about my driving."   [Back to Prevention: mental health is the absence of mental illness.]

     The essence of what has been called "depression" is that the driver acquires some knowledge of driving and of the world through the driving instructor, but a dependency remains between the driver and the driving instructor so that if the driving instructor is absent, the driver feels incompetent and lost, as in "depression". The driver may make a determined attempt to explore the world as if nothing has changed, but this tends to be frantic and unpredictable, as in "mania".

THE STRUCTURE AND FUNCTION OF THE BRAIN.

           General outline, with a notional example.

     The brain comprises a cerebrum, inclusive of two cerebral hemispheres (CH), and also a cerebellum, inclusive of two cerebellar hemispheres (CBH), and a brainstem (BS), which is continuous with the spinal cord below. The cerebral hemishperes are connected by a large bundle of nerves, the corpus callosum (CC). Each cerebral hemisphere is divided into lobes, specifically the occipital lobe (OL), the temporal lobe (TL), the parietal lobe (PL), and the frontal lobe (FL), which has both outer (OFL) and inner (IFL) parts.

Figure four

Deep within each cerebral hemisphere are three basal ganglia, specifically the caudate nucleus (CN), the putamen (P), and the globus pallidus (GP), and, central to these, a thalamus (T). A hypothalamus (HY) is below the front of each thalamus, and is connected with a substantia innominata (SI), a hippocampus (HI), a stria terminalis (ST) and an amygdala (A). The brainstem is behind the hypothalami and below the thalami and extends to the top of the spinal cord, and comprises on each side, a midbrain (MB), a pons (PO) and a medulla oblongata (MO). All these structures are connected to one another by a diffuse reticular network of nerves. Figure four shows a front view, while Figure six shows outside and inside views.
     A young man of twenty-five, John, is asleep in his suburban flat. It is 7.30 am on a late September morning. John is awoken suddenly by a loud noise. Angrily, John sits up, throws off his bed-clothes, stands up and approaches his bedroom window, where he opens the curtains and peers out. The loud noise has activated the diffuse reticular network of nerves of John's brain, specifically those reticular nerves that accompany the auditory nerves, which in turn have activated the inferior colliculi in the midbrain. Initially, John's movements are being controlled by the superior colliculi, in conjunction with the cerebellum, which has stimulated spinal nerves to increase muscle tone. Potential movements are reverberating in a loop between the midbrain and the pons. John's anger is reflected in activation of his amygdalae. Initially, John's responses are being determined by his immediate sensory perceptions, but these are starting to reverberate in his hippocampi, where they are becoming short-term memories.
     Having thrown off his bed-clothes, John has started to feel cold, and as the cooled blood from his limbs circulates to his brain, his hypothalami produce constriction of his peripheral blood vessels through descending fibres to the sides of his spinal cord, and thus to the peripheral nerves to his blood vessels, with consequent reduction in heat loss. The same circuitry is generating a degree of anxiety, as the hypothalami stimulate the release of adrenaline from the inner parts of the adrenal glands, which are on either side of the vertebral column, on top of the kidneys. The advent of light through the curtains has started to alter John's hormones, with decrease in his melatonin and increase in his cortisone and in his testosterone.
     John's approach to his bedroom window was controlled by the superior colliculi in the midbrain. The wave of reticular activation now reaches the thalami, so that sensory, motor and visceral activity are coordinated from inside the brain, rather than just elicited separately from outside the brain. Thus, the sensation of cold activates the back, sensory thalami, through spinal nerves that originate in skin receptors. The cerebellum updates the front, motor thalami with current, actual movements, while potential movements are now signalled to the front, motor thalami by an extended loop that includes not only the midbrain and the pons, but also the basal ganglia. Having been activated by anger, the amygdalae have stimulated the inner, visceral thalami. The immediate sensory perceptions, having reverberated in the hippocampi to become retrievable, short-term memories, are now starting to enter the outermost memory circuits of the lobes of the cerebral hemispheres, where they will be consolidated as long-term memories, under the influence of the substantiae innominatae: the loud noise will be associated with the abrupt awakening and with the reactions of anger and of anxiety.
     Such is the intensity of John's anger at this untimely interruption that each amygdala has taken not only the indirect, thalamic route to the lobes of the brain, but also the quick, direct route through a hooked bundle, that is the uncinate fasciculus, the angulation of which enables connection between each amygdala below and behind, and each frontal lobe above and in front.
     The wave of reticular activation now reaches the lobes of John's cerebral hemispheres, both directly through reticular fibres and indirectly through the thalami. Given that the initial stimulus was a loud noise, there are relatively intense foci of activation in the auditory, temporal lobes, mediated in part by the sensory thalami. Given that John's initial, emotional response was one of anger, there are intense foci of activity in the cingulate lobes, mediated in part by the visceral thalami. The amygdalar quick response has stimulated the inner, front part of the frontal lobes through the hooked bundles. The visual, occipital lobes have been stimulated by the light, while the back parts of the parietal lobes are starting to orchestrate movements, inclusive of eye movements, and the front parts of the parietal lobes are mediating John's body image in the registration of cold. The back parts of the frontal lobes are contributing, with the parietal lobes, to the control of movements in general and of eye movements in particular. These lobes of the cerebral hemispheres are communicating with each other through the corpus callosum and also through their outermost, memory circuits. John realises that he is sniffing for gas, and recalls that on a previous occasion, a loud noise that had awoken him suddenly had been due to an explosion of gas. At that moment, the perception of a loud noise is interacting with the memory of a previous loud noise to become an apperception, which is determining John's behaviour.
     Hitherto, a wave of reticular activation has spread reactively from below upwards throughout John's brain. Now, John will take responsibility for his behaviour as his frontal lobes start to orchestrate his brain from above downwards.
     In the first three examples below, John's behaviour is determined by his memories and by his emotional and visceral responses, in the absence of any further sensory input.
     John shrugs his shoulders, closes the curtains and muses: "Not my problem.". John lies down on the bed and pulls up his bed-clothes. This is regression, because John is failing to behave responsibly. Reticular activation starts to decrease. Reverberations, both motor and memory, start to slow. The cerebellum signals to the spinal cord to reduce muscle tone. Amygdalar activation diminishes. The warming of John's limbs by his bed-clothes produces a sensation of warmth through the sensory thalami and then in the body images of the parietal lobes. The resumption of darkness is followed by increases in melatonin with consequent decreases in cortisone and testosterone. Adrenaline levels diminish.
     John's anxieties about a gas explosion overwhelm him. John thinks about turning off the central heating to extinguish the pilot light. John dithers for what seems like ages and is distracted by palpitations and by pins and needles in his hands and feet. John then 'phones 999, whereupon he cannot remember if he has turned off the central heating when asked by the operator. Reticular activation is intense. Potential motor responses are those of flight. The cerebellum signals to the spinal cord to increase muscle tone, but because of John's uncertainties, his flexor muscles and his extensor muscles contract alternately, to produce a tremor. John is finding it difficult to organise his thoughts, and to keep images of personal injury and death out of his mind. Adrenaline levels are extremely high and are affecting the cardiovascular and respiratory centres in John's medullae oblongatae, causing a very rapid heart rate and respiration that is so rapid that it has altered John's blood chemistry and thus his peripheral nerves.
     Things have not gone well for John over the last couple of years. John's fiancée of two years ended their engagement a year ago, and rumour has had it that she married recently. Having been unemployed for a year, John has just commenced a probationary post at the local bank, but the Manager is an overbearing, irritable man. John's anger at these vagaries compounds his anger at having been awoken so rudely, and he bangs his now warm, perspirant fist on the bedroom wall, shouting: "Show some respect!". Reticular activation is particularly intense on the inner sides of John's brain. The amygdalae have transcended the inhibition afforded by the hooked bundles from the inner, front parts of the frontal lobes. The visceral thalami and the cingulate lobes are very active. Potential movements are those of hostility, and John visualises shouting: "Show some respect!" in the face of the Bank Manager. The cerebellum is distributing increased tone to the extensor muscles of John's trunk, thereby to stand up and fight. Adrenaline levels are high, and are activating the sweat glands.
     In the next three examples, the outer, front parts of the frontal lobes orchestrate further sensory input as John surveys the scene through the opened curtains, and this input influences John's subsequent behaviour.
     Across the road, in front of the Newsagent's shop John sees and hears a young lad picking himself up from underneath his felled bicycle. The Newsagent and passers-by are giving assistance. A bag of newspapers has started to empty over the pavement. Dolefully, John returns to sit on his bed, reflective of past, personal memories of similar mishaps. John feels a pain in his left knee. Reticular activation starts to decrease. Reverberations, both motor and memory, slow. John's cerebellum distributes increased tone to his flexor muscles and reduced tone to his extensor muscles, enabling John to assume a rather hunched posture on his bed. John finds himself rubbing his left knee as he recalls a particular incident when he injured that knee during a newspaper round ten years' previously. There are consequent foci of activation in the sensory thalami and in the body images of John's left knee in his parietal lobes. Adrenaline levels are falling, while prolactin levels are rising, protectively.
     At the entrance to the local supermarket, a young woman is standing shaking her clenched fists, and is screaming. The young woman's shopping bag has burst and her onions are rolling down the road. Now, this young woman has just moved into the neighbourhood, and John has found her rather attractive. A smile plays gently on John's lips, and he readies himself to give assistance, testosterone ascendant. Reticular activation starts to decrease, and reverberations, both motor and memory, slow. The cerebellum distributes increased tone to John's flexor muscles and reduced tone to John's extensor muscles, protectively so. Images of good times with his former fiancée start to come into John's mind. The sensation of cold is replaced by a rather ticklish feeling coming from his pelvis, and there are foci of activation in the body images of his genitalia in his parietal lobes. As well as the rise in testosterone, there is a fall in adrenaline and a rise in prolactin, protectively. The hypothalami reduce amygdalar arousal, and thus anger, through the striae terminales.
     John's attention is taken by a light being switched off. Glancing at the car park, John sees to his dismay that a large, rather posh-looking car is in contact with the back of his own humble vehicle. The driver has disembarked and is surveying the damage. Furtively, the driver looks around, and then gets back into his car quickly and drives off, only switching on his lights when some fifty yards away. John's anger is incandescent, but is tempered by the realisation that the driver is none other than his current employer. John is stymied. Part of him wants to go to the bank immediately and confront the Manager with his carelessness and his dishonesty. But this job has been hard to come by. This Manager is not someone who would be objective about an employee to whom he felt behoven. Momentarily, John feels dizzy, and realises that he has been holding his breath. After what seems like an age of vacillation, John determines to inhibit his natural responses, at which point tremor becomes tension. Reticular activation is particularly intense on the inner sides of John's cerebral hemispheres. The activation in John's amygdalae is matched by extremely high levels of inhibition delivered by the inner, front parts of the frontal lobes through the hooked bundles. The conflicts reverberate around and around in John's cingulate lobes. Contradictory motor responses circulate backwards and forwards through the extended loop of the basal ganglia, the midbrain and the pons, seemingly challenging the outer, front parts of John's frontal lobes to make a decision. The cerebellum is distributing increased tone to the extensor muscles but at the same moment the cerebellum is distributing increased tone to the flexor muscles, the movement of all of which is inhibited, so that John's stymied immobility is due to a generalised tension state. Images of triumph over the Bank Manager are offset by memories of inactivity and of penury. Adrenaline levels are so high that they are affecting the respiratory centre in the medullae oblongatae, with consequent breath-holding, and then dizziness.
     Muscles contract because of the release of chemical activators from the ends of nerves. Over the next few months, John will experience multiple episodes when he is on the verge of giving vent to his anger to the Bank Manager, but every time, John will inhibit his responses for the sake of his job. Such muscular inhibition requires the release of chemical inhibitors to offset the chemical activators and thereby block the muscular contractions. The chemical activators and the chemical inhibitors are made in nerves by proteins called enzymes, which in turn are produced by ribonucleic acid (RNA), under the influence of chemical formulae held by deoxyribonucleic acid (DNA), known as genes, in the nuclei of the nerves. How many episodes of personal inhibition over what period of time will be required before the chemical inhibition starts to work backwards and affect the enzymes, then the RNA, and then the DNA? Is there a danger that this inhibition of natural responses at work will start to affect other areas of John's life? Let us suppose that after a year's restraint John secures a promotion to another branch. How long will it take for John's natural responses to return, so that he can relate spontaneously to authority figures? The answer is probably about six months if bereavement is anything to go by, because that is the average time required for the reconfiguration of responses after the death of a partner for whom the responses had been configured in the first place, so as to make the relationship workable.
     What would happen chemically if this inhibition of natural responses endured in a five year-old child?
     What would happen chemically if this inhibition of natural responses endured in a five month-old child?

          The cerebral hemispheres.

     The cerebral hemispheres are situated above the cerebellar hemispheres.

     Each cerebral hemisphere is divided into lobes (2674), specifically the occipital lobe (OL), the temporal lobe (TL), the parietal lobe (PL), and the frontal lobe (FL), which has both outer (OFL) and inner (IFL) parts.

     The inner side of each cerebral hemisphere mediates personal responses (232) (1079) (687) (1017) (2522) (2873), many of which come from the cingulate lobe (CL) (922) (528) (234) (235) (529) (19) (559) (2147) (2595) (2688) (2903) (2913), which is formed from parts of the temporal, parietal and frontal lobes. There are connections with areas that contain body images for pain (876) (1746), touch (469) (1596), temperature (2528), and visceral sensations (405) (406) (651) (1264) (416) (525), and with areas that generate motor responses (1048), and visceral responses (20) (233) (326) (416).
     The inner side of each cerebral hemisphere is associated strongly with personal identity. By way of contrast, the outer side of each cerebral hemisphere is associated strongly with auditory (960) (1277) (2390) (470); (908); (21) (1694) and visual (574) (960) (2377); (2249) (2474) (2678); (882) (883) (1890) (2314) (2359) (2455) (2758) (2807) (2836) (2849); (1786) (2849); (21) (1694) representation of the outside world, including personal space (1833).

     There may be a unique, cellular basis to personal responses, of comparatively recent evolution (596), perhaps in relation to facial expression (1668) (2268).

     Each cerebral hemisphere has sensory awareness that can become focused; (410) (22) (934) (2585); (1239) (555a) (555b) (1245) (2867) (961) (2907) and that can evoke past sensory experiences (P, pages 164-168) (23) (730); motor responsiveness (1459) (1048) (1049) (930) that can become focused (2334) (2521); (24) (1050) (932) (2173) and that can evoke past motor responses; body images (879) (880) (886) (895) that can become focused (1518) (868) (1195) (2655) (2678) and that can evoke past body images (25) (26) (898), inclusive of a body image for pain, that can become focused (920) and that can evoke memories (921) (28) (27) (1972). Multiple body images mean that any one body image can be interrupted to receive new sensory stimuli without overall discontinuity. The body image can be given external spatial coordinates, so that one sees oneself through someone else's eyes (1351) (1738). The inner side of each cerebral hemisphere evokes memories of personal responses, pain and visceral sensations.
     Sensory integration occurs in the cerebral cortex (2912) (2475), within the sense of vision (1390) (1330) (1140), and between the senses of taste and smell (1260), of taste, smell, touch, audition, and vision (1720), of touch and vision (1855) (2121) (2710) (2810), of touch and audition (1979) (1980), of touch, audition and vision (1237) (2450), of vibration and vision (2122), of balance and vision (1831), of motion and vision (2541), and of audition and vision (1336) (1171) (1694) (1748) (1854) (1962) (2771).
     Sensory discrimination occurs in the cerebral cortex, within the sense of touch (1249) (2464), of audition (1236) (1245) (1647) (2540), and of vision (1291) (1292) (1286) (1994) (2275), and between the senses of audition and vision (1748) (2556). Sensory discrimination has been timed (1293) (1245).
     Sensory attention can be divided (1355) (2620).
     Sensory to motor transformation occurs in the cerebral cortex (1805) (2233) (2125) (2248) (2586) (2668) (2742).

     Visceral sensations come from the viscera, that is the internal organs, whereas somatic sensations come from the soma, that is the body (814).
     The outer side of each cerebral hemisphere is invaginated to form the insula, which is formed from parts of the temporal, parietal and frontal lobes, and which is associated with pain (876), touch (1596), taste (405) (1264), visceral sensations (406) (1595) (1603) (525), visceral responses (416) (2904), and rewards (2762).
     The horizontal area between the convex outer frontal lobe (OFL) and the vertical inner frontal lobe (IFL) overlies the eye cavity and is associated with taste (1124) and smell (1125), through respective sensory nerves (1126) (1127). Changes in taste may be mediated by the learning (1959) (2015) (2365) and reversal learning (1194) that are attributed to this particular area, which has been distinguished from the ventral IFL (233) (1430) (2255), and from the cingulate lobe (1470). Delays and rewards are mediated here (1025) (2303) (2629) (2658) (2795).

     Each cerebral hemisphere controls the opposite side of the body, which balances the control of the same side of the body by each cerebellar hemisphere. However, some control of the same side of the body is possible by each cerebral hemisphere (972).

     The cerebellum of cartilaginous and bony fishes is comparable in size with the cerebrum.

     Each cerebral hemisphere is dominant for different activities (1278) (29) (686) (2281). For example, the left cerebral hemisphere is dominant for motor activities, while the right cerebral hemisphere is dominant for sensory activities (594) (1251) (1275) (2083). The left hemisphere is dominant for verbal memories, while the right hemisphere is dominant for visual memories (923). Sensory awareness diminishes during motor acts (59) (60) (976), so that dominance may have evolved to allow one cerebral hemisphere to remain fully aware while the other cerebral hemisphere acts. A likely corollary is that motor responsiveness diminishes during sensory focus, and, again, dominance would enable both activities to be maintained concurrently. Dominance is thus a form of specialisation (529) (1238) (1230) (2471), with related cerebral asymmetry (380) (560) (1560) (2072) (2662) (2725) (2806), which increases the range of activities, both in safety (266) (529), and in vigilance (1586). The transition from arboreality to terrestriality may have enabled laterality (2271) (2776). It is likely that in immediate danger, symmetry prevails, so that the danger is given undivided attention. Symmetry may be related to gender (1942) (1845) (2042) (2210), and to sexuality (2508).

     Dominance may affect the threshold for muscular stimulation (2353).
     Dominance varies with age (1077) (2364). Somatic dominance applies to eyes and to feet, as well as to hands (1288) (1289).
     Senescence may bring asymmetry, and related symptoms (1234). Asymmetry has somatic and hormonal correlates (1283).
     Concepts activate the front of the brain, whereas percepts activate the back of the brain (912).
     Timed control has activated the language areas of the left cerebral hemisphere (2068).
     Letters and symbols show common features across languages, and these appear to reflect the contours of natural scenes (744) (1122). Numeracy has been studied in birds (248), in monkeys (1161) (1619) (2060) (2178) (2592), in human infants (1347), and in human adults (2165). Reading is a function of multiple circuits, both during (1692) (1880), and after (1021) (2264) (2395) development. Rhyming and spelling have been localised (1328).
     The lack of specialisation that has been described in schizophrenia may reflect apprehensiveness (861).
     The contrast between the inner side and the outer side of both cerebral hemispheres, as distinct from the contrast between the two cerebral hemispheres, has been developed in a model of creativity (1585).

     The inhibitory focus of the social and educational process is directed more at the verbal activity of the left cerebral hemisphere than it is at the acoustic activity of the right cerebral hemisphere, which is why the guitar is a symbol of individuality in adolescence, and why the visual world is seen differently by the right and left sides of the brain (1133).

     Communications within each cerebral hemisphere are facilitated by bundles of nerve fibres that connect its lobes (971) (1987), and these may be part of the intermediate step between perception and execution of gestures (989).
     Communications between the two cerebral hemispheres are facilitated by a large bundle of nerves that connects them, the corpus callosum (1055) (240) (1987) (1904) (2320) (2925). One cerebral hemisphere can inhibit the other cerebral hemisphere so as to produce a unilateral motor response (959). Reduction of the inhibition between the two cerebral hemispheres has produced a more rapid motor response (1838). The two cerebral hemispheres can work together in sequence, when one cerebral hemisphere acts on the environment and then the other cerebral hemisphere monitors the effects of those acts on the environment and modifies subsequent acts accordingly (30) (1826). Perception may be facilitated by contrast enhancement between the two cerebral hemispheres (1057). The stimulation of one cerebral hemisphere by the other cerebral hemisphere is seen when humans talk to themselves or to their pets, and also when they participate in soliloquies with other humans. For a more detailed, cellular illustration, see Brain cells.
     Communications within each cerebral hemisphere have been compared with communications between the two cerebral hemispheres (2221) (2849).
     The corpus callosum may be reduced in size in schizophrenia (2462).

     Each cerebral hemisphere has an outer layer of nerve cells called the cerebral cortex.

     The outer surface of each cerebral hemisphere has a neocortex of six layers, while the inner surface of each cerebral hemisphere has a mesocortex of five or six layers above, and an allocortex of three layers below. See these references for studies of architecture (2175) (2166), of precise microarchitecture (945) (1284) (2107) (2684), of cell types (945) (2051) (2461) (2685) (2757), of cell development (946), and of spontaneous activity (1775).
     The cells appear grey, compared with the nerve fibres, which appear white. Some unlikely associations have been found between white matter and mendacity (662) (1848), and between neocortical volume, that is grey matter plus white matter, and deception (2709), while less unlikely associations have been shown between grey matter and chronic back pain (1507), and between grey matter and social network size (2804). Grey matter has been seen to increase during learning (990) (1843).
     The nerve cells are surrounded by connective tissue cells, called glia (2352) (2424) (2410) (2590), and these have been thought to support metabolic demands (2407). The ratios between glia and neurones in human brain structures are similar to those found in other primates (2559).
     Primate brains have a larger number of nerve cells than rodent brains of similar size (1887). Within primates, absolute brain size has been shown to be a better predictor of cognitive ability than relative brain size (2040). Humans share some common features of the temporal polar cortex with other primates (2915). Humans have a unique cellular network compared with chimpanzees (2799), but there is a developmental similarity (2910) Within humans, cerebral volume has correlated with verbal ability and with visuospatial ability, subject to sex and to handedness (2042).
     There are cells in the cerebral cortex that become active both when the organism sees another organism produce a response, and when it produces that response itself (31) (32) (2171) (2415) (2920). These cells are likely to be a basis for learning (1664) (2225), and they afford explanations for lip-reading (1078), for shared body images, for phantom limbs (1240), for enactment of someone else's wishes, for imitation (2785), for protective responses, and for division of labour within the animal kingdom (245) (341) (577) (804) (2010). Studies of mirror neurones in developmental disorders should address the actual relationship between the patient and his or her parents (1669), and, in particular, the degree to which each parent can mirror the patient's responses back to the patient, both in terms of motor responses, such as folding of the arms, and also in terms of what those motor responses are likely to mean to the patient; thus, the parent would accompany mirrored folding of the arms with a facial expression, such as sad or happy or angry. The predictions to be disproved, using an operant model, are that there will be less activation of identical areas of the brains of children with developmental disorders and the brains of their parents, than between the brains of normal children and the brains of their parents, not only when the child's responses follow the parent's responses, but also when the parent's responses follow the child's responses (1739); and also that the differences between the brains of parents of children with developmental disorders and the brains of their children persist when those parents are studied with normal children, and that the differences between the brains of children with developmental disorders and the brains of their parents reduce when those children are studied with the parents of normal children.
     When cells in the cerebral cortex become active as the organism sees another organism produce a response (33), this is an expression of memory (263), and then of preparatory motor, also called premotor, behaviour (1787). Similar considerations apply to cells that become active when the organism hears sounds related to actions (1797), and sees objects related to actions (1935).
     There are cells in the cerebral cortex that become active when the organism sees another organism receive a response (372), and this is an expression of memory (373) (1700), and then of preparatory motor, also called premotor, behaviour (374). Terms such as empathy (375) (376) (353) and schadenfreude (377) (2039) cloud the issues, and enable findings which are likely to lack specificity (1678).
     Given that perception occurs in cells in the inner layers 4 to 6 of the cerebral cortex and that memory of perception occurs in cells in the outer layers 1 to 3 of the cerebral cortex, and given that one's self is represented by the mesocortex on the inner side of both cerebral hemispheres, while others are represented by the neocortex on the outer side of both cerebral hemispheres, then one's perception of another person perceiving one's self will make a complete circuit between cells in the inner layers 4 to 6 of the mesocortex on the inner side of both cerebral hemispheres and cells in the inner layers 4 to 6 of the neocortex on the outer side of both cerebral hemispheres, while one's memory of one's perception of one's self by another person will make a complete circuit between cells in the outer layers 1 to 3 of the mesocortex on the inner side of both cerebral hemispheres and cells in the outer layers 1 to 3 of the neocortex on the outer side of both cerebral hemispheres. It follows that the more often one has perceived one's self to be perceived by others and the more of one's self that one has perceived to be perceived by others, then the more one's self will be represented by the cells in the outer layers 1 to 3 of the cerebral cortex, and by a complete circuit between the cells in the outer layers 1 to 3 of the mesocortex on the inner side of both cerebral hemispheres and cells in the outer layers 1 to 3 of the neocortex on the outer side of both cerebral hemispheres. Insofar as the memory is of someone else's look of concern in response to one's facial quiver, and is thus in one's mind's eye, then the complete circuit will be between the cells in the outer layers 1 to 3 of the mesocortex on the inner side of both cerebral hemispheres and cells in the outer layers 1 to 3 of the neocortex of the occipital lobes, which is the cellular specification of seeing one's self through the eyes of another person, because one has seen another person see one's self. Insofar as the memory is of someone else's words of comfort in response to one's plaintive cry, and is thus in one's mind's ear, then the complete circuit will be between the cells in the outer layers 1 to 3 of the mesocortex on the inner side of both cerebral hemispheres and cells in the outer layers 1 to 3 of the neocortex of the temporal lobes, which is the cellular specification of hearing one's self through the ears of another person, because one has heard another person hear one's self. Complete circuits between mesocortex and neocortex reduce the likelihood of splits in the brain, whether they are within cerebral hemispheres or between cerebral hemispheres, because of the instinctual input to the mesocortex and the perceptual input to the neocortex. [Back to Introduction if required.]

     For historical perspectives of the cerebral hemispheres, see references (616) and (1160).

           The cerebellar hemispheres.

     The cerebellar hemispheres are situated below the cerebral hemispheres and behind the brainstem, and they are connected by the central vermis, with which they constitute the cerebellum.

     Each cerebellar hemisphere controls the same side of the body (2734), which balances the control by each cerebral hemisphere of the opposite side of the body: if one side of the brain is injured, both sides of the body can still be moved.

     The cerebellum of cartilaginous and bony fishes is comparable in size with the cerebrum.

     The cerebellum coordinates movement (34) (500) (676) (2320), including eye movement (2486), through the use of immediate sensory feedback stimuli to refine motor responses (1303) (1306) (1597) (1706) (2068) (2801), which otherwise would be based on remembered motor responses to similar stimuli in the past (35) (36). The lack of such refinements is evident in the motor approximations of drunkenness, in which state talking and walking are based largely on memory, as distinct from perception.
     Immediacy may be served by connections between brain cells that are electrical (535), and implicitly quicker, rather than chemical, and implicitly slower, although the immediacy may bring a loss of precision. Chemical connections may occur between neurones and blood vessels (673) (1192) (1304) (1371) (2355).
     The cerebellum receives immediate sensory stimuli from the spinal cord (37a) (37b), and from the brainstem (355) (889), while at least some of the remembered responses to the cerebellum are relayed from the occipital, temporal (440), parietal (38) (1556), and frontal lobes of the cerebral hemispheres, through the pons in the brainstem (39) (1031) (2226).
     Responses that have been unproductive in the past may be inhibited by the cerebellum; this minimises the organism's responses to predictable sensory events, which emphasises the importance of an immediate, on-line, brainstem review of sensory events to ensure that they are indeed the same, predictable events that occurred before.

     The cerebellum detects the operation of an outside force on the organism, through the occurrence of muscular stretch in the absence of prior, explanatory, muscular contraction. When the organism contracts its own muscles, the stimuli that cause the contraction are copied to the cerebellum, where they offset any activation caused by muscular stretch consequent upon the contraction, which activation is recorded in the cerebellum; the absence of the offset, or corollary discharge, indicates that the muscle has been stretched by an external force (41) (2761) (2786).

      Memories of past motor responses to sensory stimuli enable visual images of motor responses (42), and play activity enables a child to acquire these images in relative safety (43) (2143) (2157, page 68) (2928). Inferences may be made about motor skills when adults play (348). The cerebellum distinguishes between actual movement and imagined movement (927), especially in its anterior area (1009).

      A child whose motor responses are inhibited habitually acquires a body image of motor responses that is less than his or her innate, that is genetic, potential. When the sex hormones of puberty surmount inhibitions, the now adolescent is faced with the problem of who is responsible for unfamiliar motor responses, for example to anger. It is extremely common for adolescents to use alcohol and recreational drugs to address this problem, because, objectively, the implementation of the unfamiliar responses during inebriety is seemingly because of inebriety, and, subjectively, it feels as if another character has been responsible. Failure to address the problem augurs the disturbances of passivity phenomena (44).
     Alcohol and recreational drugs may act as deterrents to social interactions (583).

     The cerebellum has an outer cortex of three cell layers (1310), and in humans, each cerebellar hemisphere contains four nuclei. The cerebellar cortex and the cerebellar nuclei have been compared and contrasted (1307) (1309) (1755).
     Within the Purkinje cell in the cerebellar cortex, coordination occurs as the electrical activity evoked by an immediate sensory stimulus offsets the electrical activity associated with the remembered response to a similar sensory stimulus (40) (1305) (1370) (1394). Presumably, the cerebellar nuclei transmit the result of the offset to the rest of the brain (1378) (1812). A similar system may enable variation of responsiveness to sensory stimuli (929). Timing is a function of alignment of Purkinje cells (2003).

     The cerebellum may participate in visceral activity (844); in cognition (950); and in working memory (950) (2463).

     The cerebellum varies in size and structure between and within vertebrate classes, for example (F, page 199) (G, pages 306-307) (611) (2269a) (2269b). The hemispheres of primates are relatively large, probably due to their manual dexterity (762). The phylogeny of the cerebellum has been studied comparatively in birds and in flying reptiles (1162).

          The basal ganglia.

      Deep within each cerebral hemisphere, lateral to each thalamus, are three basal ganglia, which produce and contain potential motor responses (45) (1781).
      Specifically, the caudate nucleus produces motor responses for the head, neck and eyes (46) (1163) (1016), the putamen produces motor responses for the body, while the globus pallidus keeps motor responses on hold until they are needed (47), when they are literally funnelled through (1201). Lack of movement may be an active process (48) (2883). Potential responses reverberate with the brainstem, specifically the substantia nigra, which also keeps motor responses on hold until they are needed (1749). The organism is thus able to select from a number of potential motor responses that are in a state of readiness (49) (2248) (2613).
      One of the meanings of stress is that the reverberant system of potential motor responses is overloaded, because input has exceeded output.
      Winding someone up includes stimulating potential motor responses while at the same time denying an opportunity to express them (356). A debrief is winding down by giving an opportunity to discharge reverberant motor responses, expressed in animals as the redirection of aggression (321), and in early Man, as laughter (565) (2796).

     The need to discharge unused muscular activity so as to reset motor units may explain the timing of participation in ritual fights between conspecifics (18), which are relatively safe (321), and may also be at least somewhat explanatory of homosexual behaviour in animals (2143), of why predators attack unpalatable prey (322), of why herring gulls pull up grass during a fight (518), of why black-headed gulls preen markedly when all three eggs are removed from their nests (519), of why dead offspring are nursed (551), and of punishment (80) (2130) (2330) (2357) (2595) (2704) (2755).

      Each caudate nucleus and each putamen include a chemical called dopamine, which translates an unmet visceral need into the motor activity necessary to meet that unmet need, through stimulation of the substantia nigra (50a) (50b) (1090) (758) and, through it, a reticular network of nerves in the brainstem and spinal cord. This reticular network of nerves controls muscle stretch receptors (2926) that can tone muscles or make them more sensitive to stretch, or both. Thus, the hungry animal can have the muscles in its neck and trunk toned, with its hip flexors also toned but its hip extensors lengthened and set to react to the slightest stretch, as it waits, poised, to pounce on its prey. This state of readiness is achievable because the dopamine nerves of the caudate nucleus and putamen that can stimulate the reticular network, send nerve branches to the globus pallidus where they activate an inhibitory chemical called gamma-aminobutyric acid (GABA) that keeps the movements on hold until they are needed (51) (1180) (997) (2311) (2677). This preparatory mode is achieved at a cost, in terms of the energy required to maintain activation of some responses and to inhibit other responses.

     The state of readiness of reverberant, potential motor responses enables basal ganglia responses to move forward in time, relative to cerebral cortical responses and to thalamic responses (925).

     The basal ganglia enable muscles to be maintained in a state of readiness and then either toned into a posture or alternately flexed and extended in movement, through the patterned activation and inhibition of the muscles' stretch receptors.
     We reset our muscle stretch receptors every night when we yawn and stretch, thereby to enable muscles to be stretched without reflex contraction during sleep (52a) (52b) (2847), and also to facilitate the deep inhalations that will induce sleep through oxidation (1538). The next morning, we reset the stretch receptors to produce a reflex contraction at a shorter muscle length as we brace ourselves and tighten our muscles (935).
     Motor response patterns can be delivered to the muscles through the spinal cord by the cerebral cortex in conjunction with the cerebellum, using chemicals which include acetylcholine. This circuit uses more of the brain than the dopamine circuit, so that it is longer, less spontaneous and less reflex (53), and thus is subject to premeditation on its way through the brain. Immediacy of response can be used to judge truthfulness in Courts of Law.
     Tension states are due to a generalised increase in muscle tone, which is sustained to the degree that pain may be caused by lactic acid, trapped nerves or torn muscles. Importantly, the muscle tone is increased symmetrically, which conveys the lack of readiness for movement.
     Trembling, fidgeting and twitching are all due to a state in which, within the basal ganglia, the drive to move the muscles through dopamine is close to surmounting the inhibitory control through GABA. However, there is no motor response pattern from the cerebral cortex and cerebellum for the basal ganglia to drive, because of a premeditated wish for restraint, implemented through inhibition of the muscles by the cerebral cortex. Remove that wish and the individual in this state can move very quickly.
     Different again is the state of restlessness in which patterns of movement, such as getting up and walking around, occur in a disjointed, fragmentary manner. Herein, the cerebral cortex and the cerebellum are delivering motor response patterns, but these are ineffective because the basal ganglia are not producing the sustained stretch reflex sequences necessary for their implementation. This state can be seen in someone who has mixed feelings about how to respond (321).

     Evidently, the cerebral cortex and the cerebellum on the one hand and the basal ganglia on the other hand have to coordinate their responses for meaningful movement to occur (36), and this requires them to be in phase with one another (1557) (54). The basal ganglia receive input from the cerebral cortex (1468d) (1449) (1063) (1165) (1130) (2245) (2820), although there is no direct reciprocal circuitry. With respect to any particular joint, contraction of its flexor muscles should be associated with inhibition of the stretch reflex of its extensor muscles, and vice versa. If the cerebral cortex and the cerebellum on the one hand and the basal ganglia on the other hand are out of phase, then tremor or rigidity will result, depending on the phase relationship, because if the cerebral cortex and the cerebellum activate a flexor to contract against an extensor in which the stretch receptor has been set by the basal ganglia to be taut, then a tremor will be initated, because the extensor will be stretched by the flexion and will itself contract vigorously and stretch the flexor, which will react with equal vigour if the basal ganglia have set its stretch receptor in a taut position; and so on (1509). If a flexor contracts against an extensor that is already contracted, then the result is rigidity, which is desirable if the intention is to maintain a posture, but is undesirable if the intention is to produce a movement. Both tremor and rigidity during movement are caused by the major tranquillisers used to treat mental illness, which drugs inhibit dopamine, and by Parkinson`s disease, in which there is degeneration of cells that produce dopamine. In both circumstances, drugs that inhibit acetylcholine may be effective, because they bring the acetylcholine and dopamine systems back into phase.
     The restoration of normal phase relationships may be the common feature in the therapeutic effects of drugs (1168), electrical stimulation (1095) (1169) (1482), and ablation (1170).

     The concept of an emotional motor system (1052) has not generalised.

     The circuitry of the cerebral cortex and the cerebellum can compensate for the circuitry of the basal ganglia when it is diseased (55) (1473) (144) (1067) or genetically weak (56) (1181). The distribution of genetic weakness of movement within the human population may explain the distribution of disorders of movement due to major tranquillisers within the human population. The delineation of genetic weakness anticipates the general use of genetic profiles prior to drug prescription to predict, and thus avoid, drug side-effects (57) (805).

     Movements can become automatic, which has been associated with a reduction in activity in the basal ganglia as well as in the cerebellum and in the cerebral cortex (968), with an increase in activity in the basal ganglia relative to the cerebral cortex (1895), and also with a change in the distribution of activity within the basal ganglia (1186) (1187) (1327). Measures of automaticity based on distractors (968) (1327) may be confounded by working memory (1331) (1333) (2406). If learned movements rather than perceived location are used to find one's way around, then basal ganglia activity increases (1164) (1188).

     The claustrum is an indeterminate collection of cells (411) on the inner side of each insula (405) (406), and it receives auditory, visual and visceral stimuli (412) (1468d) and transmits to the neocortex (413), to the mesocortex (495), to the allocortex (1468b), and to the thalamus (1496), suggestive of a correlative function.

     The dorsal and ventral parts of the basal ganglia may process different types of stimuli (2631) (2906) (2921).

     Shorter latency pathways may include the claustrum (411) (413), and the lower, ventral parts of the basal ganglia (721) (722) (1788) (2562), while the longer latency intra-thalamic pathways may include the upper, dorsal parts of the basal ganglia.

     The basal ganglia have been conserved throughout vertebrate phylogeny (2715), with variations (C) (1182) (1183). The functional analogy is of preparatory motor, also called premotor, behaviour.

          The thalami.

     Each thalamus is situated deep within the cerebral hemisphere, beside, and central to, the basal ganglia. Below the thalami are the hypothalami in front and the brainstem behind. Each thalamus is connected with the cerebral hemisphere on the same side, and, to a lesser degree, with the cerebral hemisphere on the opposite side (2530). Consistent terminology of the thalamus has been elusive (70) (617) (618) (2019) (2451) (2745).

     Each thalamus can determine the degree of sensory, motor and visceral activity that passes through it at any moment (58) (986). Suppose that, on the threshold of its habitat, an animal surveys its territory in a state of vigilance. The animal then forages, that is it explores the territory in a state of anticipation. The sudden appearance of a predator results in fight, flight, or frozen immobility (2338). Having survived the encounter, the animal returns to its habitat to feed, excrete, rest, mate, and sleep. In this example, at any moment an animal can be in one of ten different states, each of which has a different combination of sensory, motor and visceral activities. Vigilance is a sensory state, with motor readiness and with visceral inactivity. Foraging is a combination of sensory and motor states (1460) (2154), again with visceral inactivity. Fight, flight and frozen immobility are motor states that are protective of the animal, to the exclusion of potentially hazardous sensory and visceral activities. When it is safe, the animal feeds, excretes (714), rests, mates (269) and sleeps (712) when sensory vigilance (285) and muscular readiness (567) have been relaxed. Feeding and mating involve different parts of the visceral nervous system, and attempts to combine these states carry hazards, for example of choking (506).

     Each thalamus is a transmission gate between its cerebral hemisphere (2531) and the brainstem (59) (60) (61) and spinal cord (1322) (1726) (1727), so that the thalamus orchestrates (62) (748) (2295) (2649) between sensory (277) (620) (63) (64) (2134) (2466), motor (65) (66), and visceral (67) (1080) (1660) (2246) modes. Within the sensory mode, both sensory integration (2523) and sensory discrimination occur (1505) (1748); (1500) (2513) (2336) (2368) (2587); (1498) (2299); (1497) (1499) (2296) (2446). Within the motor mode, spontaneous and evoked responses have different thalamic circuitry (68) (69) (2571).
     It is likely that gamma-aminobutyric acid (GABA) is participative in thalamic transmissions (1493).

     Stimuli may reach the cerebral cortex without traversal of the thalami (1250), and responses may pass from the cerebral cortex to the spinal cord without traversal of the thalami (926); these extra-thalamic pathways have a shorter latency than intra-thalamic pathways, but they are not orchestrated to the same degree (1867). It is likely that fight, flight and frozen immobility are extra-thalamic (288) (850) (289) (471), given the need for urgency, whereas vigilance, exploration, feeding, excreting, resting, mating and sleeping are likely to be intra-thalamic, given the need for orchestration. It is likely that juries use response latency to judge truthfulness, if not spontaneously, then under judicial direction. Legal intent becomes anatomically accessible through the likely relationship between response latency and degree of premeditation (2643) (2680).
     The shorter latency, extra-thalamic pathways may include the claustrum (411) (413), and the lower, ventral parts of the basal ganglia (721) (722) (1788) (2562), while the longer latency intra-thalamic pathways may include the upper, dorsal parts of the basal ganglia. The dorsal and ventral parts of the basal ganglia may process different types of stimuli (2631) (2906) (2921).

     Each thalamus can disconnect and then reconnect its cerebral hemisphere and the brainstem during sleep (81) (1510), and during hibernation (2195). Disconnection allows the nerve circuits of the cerebral hemisphere and of the brainstem to reverberate independently of each other (1074) (825) (2503), so that the cerebral hemisphere is able to process unused motor responses without activation of the brainstem and the brainstem is able to process unused motor responses without activation of the cerebral hemisphere (82) (1410). Reverberant sensory stimuli and memories can be processed without having to compete with new sensory stimulation. This is the refresh mode of the brain (1818), and its effects have been shown during the day (1594), overnight (84), after 12 hours (1539), after 24 hours (2047), after 48 hours (1540) (2252), after 3 days (83), and after 6 months (2252). Repeat of the same sensory stimulation during sleep, as when awake, may improve memory (1872). The type of sleep may reflect predation risk (1634) (2327).

     The need for orchestration of the different activities afforded by the brain (71) is illustrated further by their sometimes opposite effects on the body. For example, during flight, the limb muscles are set to react to the slightest stretch, the trunk muscles are toned, the heart rate is rapid, the airways are dilated and breathing is deep and rapid, vision is set for distance, secretions are dried, bowels are inactive and there is no sexual activity: during feeding, the limb muscles are set to tolerate stretch without contraction, the trunk muscles are relaxed, the heart rate and breathing are slow, vision is set for nearby (832) (779), salivary and alimentary secretions flow, bowels are active and there is no sexual activity.
     It is likely that the sensitivity of the outer hair cells of the cochlea (2137) (2138) (1345) (1263) (2177) (2013) is set according to sensory, motor, and visceral activity.
     Spontaneous eye blinks have been shown to be controlled by humans, to minimise the chance of losing critical information (2614).
     It has been contended that different visceral responses are controlled by different cerebral hemispheres (1029), although this seems to be based largely on cardiovascular responses, for example (1033), and on specious arguments, for example, that excessive arousal in the left hemisphere in response to negative emotional stimuli is evidence of specialisation of the left hemisphere in positive emotions (1034), and that excessive sweating on the paralysed side after a stroke (1035) allows the inference that different cerebral hemispheres control different visceral functions in health (1029).

     An animal's defence against potential danger includes immobility, which implies diminished respiration, so that the sound of its breathing does not give away its location to the predator. Anaerobic respiration is adaptive in this respect. Hyperventilation will occur because of the hypoxic drive to chemoreceptors, and may determine the moment of fight or flight (72). One of the more surprising pieces of advice imparted by doctors is that an anxious person who is overbreathing should be encouraged to re-breathe from a paper bag. Not only does this go against the grain, but the poor physiology takes away what little breath one has left. Medical opinion is that anxiety causes hyperventilation that, in turn, causes hypocapnia, hence the advice to re-breathe from a paper bag and increase the levels of carbon dioxide (73). Conspicuous by their absence are questions about what part hypoxia has had to play, and when, in evolution, we switched from being animals with bated breath to being humans with hyperventilation. Until proven otherwise, hyperventilation in humans should be assumed to be secondary to hypoxia consequent upon bated breath, and should be alleviated through deep, slow breaths, and not worsened by moving the same column of air up and down the dead space. The management of hypocapnia and its consequences should be deferred until after the hypoxia has been addressed. When the anxiety is associated with depersonalisation, hypoxia should be considered as a possible explanation.

     Modern stress may include too much sustained sensory and motor activity with too few punctuations by visceral activity, including digestion, so that the related high fat levels are unsurprising. The social structure of the habitat and of the territory may be influential in the outcomes of stress (973) (974); (310) (803); (2516)(2506) (2492) (2713), and vice versa (2203) (2468).

     Proactive and reactive stress coping styles have been identified (2200). The parents of a child with schizophrenia may have a reduced risk of cancer (1849).

     One of the meanings of stress is the lack of activity in circuits that pass from cells on the inner sides of the cerebral hemispheres to cells on the outer sides of the cerebral hemispheres, relative to activity in circuits that pass from cells on the outer sides of the cerebral hemispheres to cells on the inner sides of the cerebral hemispheres. The discrepancy may be due somewhat to the differential responses of the people on whom we depend to activate the cells on the inner sides of our cerebral hemispheres. Sufferers from tension headache may wish to experiment.

     The thalamus has been implicated in hysteria (1204), a reference that was absent predictably from a recent reductionist review of the thalami (2518), written by someone who had little knowledge of psychiatric patients. EG Jones' ignorance of psychiatric patients and his perfunctory attitude to psychiatry were well shown in an otherwise erudite and instructive article about calcium channels in the brain (2519), wherein Jones perpetrated the offensive metonymy of "schizophrenics", and cited, as evidence of impaired cognitive control in schizophrenia, a study in which the patients were taking medication, in which there was no control group with mental illness, and in which there was no reference to diagnostic reliability (1770).

     The thalami deliver the instinctual activity of the brainstem and of hypothalamic structures to the cerebral hemispheres, including the eye-fields of the frontal lobes (74) (1508), so that the other occupants of the habitat and of the territory are characterised, (75) (474), for example as hostile (76) or as in need of protection. This transmission of sensory information from the periphery to the cerebral cortex is first gear (1503) (597) (2335). Relay of information from one cerebral cortical area to another is second gear (598). The gears are operated by the driver (1387) (1853) (2751).

     Animals, including humans, demarcate their terriories (1185). Animals use secretions and excretions. In recent years there has been a realisation by human animals that there may be a connection between excretions and cigarette smoke. Insofar as the smoker gets the benefit of group membership without the cost of conformity, he or she is a social cheat, and as such, has antecedents, both unicellular (16) (1184) (77) (776) (2192) and multicellular (2379).

     The protectiveness of animals, including humans, towards unknown adult animals is, at least to some degree, territorial, in that the demarcated territory is kept safe (1814), and therefore so are the other animals in it; thus what has been called altruism (78) (79) (80) has primitive origins (95) (816) (75) (253) (1760) (1814) (1884). It is not surprising that preferences may be shown to animals that resemble oneself (733) (790) (1815), and that antagonism may be shown to animals that differ from oneself (1639).

     Responses to the releasing stimuli proposed by ethologists (K), are likely to be conditional upon perceived safety (545).

          Hypothalamic structures.

     A hypothalamus is below the front of each thalamus and in front of the brainstem, and it sends branching nerve fibres, and thus identical messages, to each of these structures, which are therefore kept in tune with one another.
     Each hypothalamus sends nerve fibres to the brainstem (1583) (654) (772) (1590) (672) (1323) and to the spinal cord; fibres to the front of the spinal cord control motor output (336), those to the side of the spinal cord control visceral output (445) (338) (337) (1600) (1601) (853) (421) (422) and those to the back of the spinal cord regulate input (338), both sensory (339) and visceral (340), including, in animals, the position of the tail (554) (1618). Some nerve fibres have branches to both the brainstem and the spinal cord (1599).
     Each hypothalamus receives nerve fibres from the brainstem (2454).
     Each hypothalamus receives nerve fibres from the retinae (395) (357) (358) and from the derivative visual nerves (2169), and transmits the influence of daylight to the brain (360) (361) (359) (362) and to the body (2348), partly through local chemical diffusion (947), and partly through the release of a chemical, melatonin (363) (364) (1762), from the pineal gland, into the circulation. The hypothalami mediate effects on appetite (365), sleep (366) (367) (368) (1146) (2386), body temperature (369) (542), sugar (791), protein (1002), fat (801), fluid (602) (603), and salt (845) (836).
     The specific circuitry entails the lateral habenular nuclei (360) (361) (362) (150) (2756) (2811) and the lateral geniculate bodies (370).
     The hypothalami participate in immune responses (85) (86) (87) (270) (1918), and thus in the cellular definition of what has been called self and non-self (741). Immune responses change over minutes and over days (1571) (1572), perhaps because the distinction between self and non-self becomes blurred. There are implications for cost (1579) (2383).
     The hypothalami orchestrate puberty (2055) (2056), sexual behaviour (523) (777) (2746), urination (micturition) (1323), lactation (759) (775), salivation and lacrimation (1101), aggressiveness (1551) (294) (775), fear (1093), defensiveness (295) (738), foraging (808), and hibernation (2195).
     The hypothalami orchestrate the release of chemicals from glands directly into the circulation (2683), often through the intermediary activity of the nearby pituitary gland. These endocrine glands do not have ducts, unlike exocrine glands, such as those that lubricate digestion, for example the salivary glands. The endocrine glands include the thyroid gland, the parathyroid glands, the adrenal glands, the pancreas, the testes, the ovaries, and the placenta (649) (2839), in addition to the pineal gland and the pituitary gland. The chemicals released are called hormones, and these influence the brain (371) (1339) (1342) (1343) (1358) (1940) (1969) (2419) (2802) (2812), the spinal cord (2548), and the body (1570) (581) (582) (1736) (2634) (2670), inclusive of variations in the body image (482) (1690).
     The hypothalami, the pituitary gland, and the adrenal glands coordinate a response to stress (1532) (1856) (2036) (2203) (2205).

     The hypothalami are themselves orchestrated by chemical signals from other parts of the brain, inclusive of the cerebral cortex (1782), the thalami (754), the cerebellum (844), and the medulla oblongata (901).
     There have been reports that growth hormone is produced in the hippocampi (792) (755).
     Leptin is a designated hormone produced by fat cells (801) (802), and is part of a circuitry that mediates arousal (846) (815) (829) (672) (2070), sexual arousal (1889), stress (835) (2100), and food intake (828) (830), which latter may be increased by humans in an attempt to lower stress levels. Related hormones are ghrelin (543), amylin (543), and adiponectin (2414).
     One hypothalamic hormone, oxytocin, has been reported to increase trust in humans when given intranasally (291), but the researchers did not attempt disproof of their "double-blind" design, which decreases trust in their report, not only because oxytocin may have a smell, but also because it affects the sense of smell (589). Another hypothalamic hormone, vasopressin, has been reported to evoke agonistic facial responses in men, and affiliative responses in women, in relation to unfamiliar faces (697), but then so does a fart. Both oxytocin and vasopressin have been described as affected by early social experiences (1373), although these were group comparisons, without change scores.
     Hormones are chemical signals within one organism. Pheromones are chemical signals between organisms (1992), and can, in principle, include tastes as well as odours (774). Pheromones have been compared with other odours (1254). Different anatomical structures have been though to mediate odours and pheromones (2079) (1719).

     Anatomically, the distinction between inner personal responses, and outer reactivity to the environment, appears to obtain in the hypothalami (739).

     Electrical stimulation of the hypothalami has been used to treat intractable headaches (823) (824) (2172).


     Each hypothalamus is connected with a number of other structures which are also below the level of the thalamus and which are thus hypothalamic in the anatomical sense.

          The substantia innominata is beneath the globus pallidus and is a diffuse area: it includes a network of cells that release acetylcholine (89) (1321) (2914), and this network coordinates brain activity when awake (90) (1285) (689) (1611) (1627) (2876) (2882), and during paradoxical sleep (91) (1206). The distribution of acetylcholine has been compared in the frontal cortex of humans, chimpanzees and macaque monkeys (2254).

          The hippocampus allows sensory stimuli, and their associated arousal, to reverberate, and to form and then evoke memories (92) (1356) (1337), which are then comparable with subsequent sensory stimuli (2243). These reverberations include visceral (93), olfactory (297) (1442) (1872), visual (94) (1397) (1950) (2735), vestibular (1446) (2293), positional (1725), and tactile (2243) stimuli, so that associations are made between the inner world of feelings and the outer world of places (95) (1461) (1443) (1435) (1640) (1870) (2008), and of contexts (96) (1820) (1945). If you feel hungry, you recall the smell of food, and in your mind's eye, you see places where you have eaten in the past.
          Some reverberations may not form memories (1475).
          The left hippocampus and the right hippocampus may have different functions (2001).
          Memories of objects (1893), of configurations (1463), of backgrounds (1286) and of odours (1257) have been demonstrated in the mesocortex adjacent to the hippocampus, and these may be stimulated by sensory input (1468a) (1466) (1448) (98). Damage to the mesocortex adjacent to the hippocampus has resulted in loss of memory for events covering decades, compared with damage to the hippocampus itself, which resulted in loss of memory for events covering approximately 5 years (1792). Autobiographical memory has been shown to be sensitive to the interview technique (1792) (2351). Surgical resection that included the mesocortex adjacent to the left hippocampus, but excluded the left hippocampus itself, has resulted in impaired verbal learning (1991).

          Electrical activity has been recorded from human hippocampi through electrodes (2720).
          The association of each sensory stimulus with a type and a degree of arousal explains why happiness brings happy memories, why sadness brings sad memories, why anxiety brings worry about the past and about the future, why a low blood sugar makes us think of food, and why fatigue makes us think of sleep: we perceive (1756) (1774) (2744) and recall (1173) through our moods. Dependent adults who lack insight into their moods tend to be led by those moods, and to imagine that the thoughts and images consequent upon those moods are the premeditated causes of those moods. Potential motor responses may be generated and then implemented, to the chaotic degree that the individual seeks out events that are associated with the same thoughts and images. Hence the importance of periods of reflection to disentangle moods, memories and actions.
          An adaptive value of moods is the demonstration to the organism that it exists (2157, page 88), thereby prompting the organism to locate itself in a dangerous world: "Where are the causes of this mood? Are they in me? Are they in my habitat? Are they in my territory? How far do I forage?" Emotional abuse of children occurs when adults locate the causes of their own moods inside those children.
          Thoughts and images that have been associated with the same mood at different times may become conflated as false memories of a single event.
          Anatomically, moods are states of arousal, each associated with nerve circuits that originate in the brainstem and then extend upwards to include the hippocampus. Each nerve circuit, and thus each state of arousal, each mood, and the related perceptions and memories, are associated with a particular chemical (1589); (986) (2297)(2029), illustrated by a drug that inhibits a noradrenaline nerve circuit, the arousal and mood of anxiety, and fear memories (1550). A brain protein, kibra, has been associated with memory (2427).
          The same nerve cell can store, at the same time, more than one type of sensory input (1265), for example, visceral input from the brainstem, olfactory input from the diagonal band and the septum, and visual input from the midbrain, so that the future occurrence of any of those inputs evokes the other types of input, in their absence, as memories (420) (492) (1828). Conditioned responses are predicated on cellular associations (1504) (1379) (1512). Recall by the cerebral cortex in the absence of sensory input requires the cerebral cortex to activate memories of sensory input into the hippocampus, which memories then activate the cerebral cortex (349) (350). Such activation increases the number of open nerve circuits and therefore increases response time, so that it is subject to perceived safety (545). Recall makes a memory fragile (1445) (1614). Repeated episodes of recall by the cerebral cortex are themselves remembered by the cerebral cortex, and can be used as cues for further episodes of recall, independent of memories of the original sensory input into the hippocampus (415) (628). Left frontal regions of the cerebral cortex have been shown to be important for recollection (1329) (2234), for recognition (910) (1598), and for recall (1598), albeit subject to variation in definitions and in experimental formats. To this writer, the more spontaneous, and thus the less latency, as in familiarity and recognition, then the more subcortical and the more allocortical are the processes, whereas the more voluntary, and thus the more latency, as in recollection and recall, then the more mesocortical and the more neocortical are the processes (1708) (1709) (1710) (2292) (2315) (2680).
          The hippocampus may be supplemented by the basal ganglia in navigation (1164) (1188) (2416), and by the cerebellum in conditioning
(2463).
          Input to, and output from, the hippocampus can be contained in reverberatory circuits (1467a) (1467b) (97) (1429) (99) (100) (1391) (2488) (2489) (2719), until it is safe, efficient and desirable to process the stimuli and action the responses (613) (1389), or until containment is no longer relevant (1864). The human organism's introspection of full reverberatory circuits is of stress, and repose or sleep may be needed to empty the circuits, for example through integration of new hippocampal associations into the cerebral cortex (1450) (101) (1398) (1404) (906) (2252). The prior existence of similar memories in the cerebral cortex enables stimuli to be processed more quickly, with less hippocampal containment (1928).
          The mesocortex between the hippocampal allocortex and the neocortex is where the organism meets the organism's representation of the world (2911) (771); (1426) (1428) (1001) (1926) (2052); (1179) (1633); (2062); (1976) (1977) (1978); (1141) (1142), and this may include the organism's representation of itself (2206) (2098) (2429). The neocortex is where the organism meets other organisms (1676).
          The hippocampus transmits directly to the amygdala (2174) (1197), and to the inner side of the frontal lobe (881) (884) (1381) (2500), which circuits may be related to foraging.
          Aging has been related to specific hippocampal cells (1436), and to compensatory overactivity in the hippocampi and in the cerebral cortices (2350).
          The curvature of the cells of the hippocampus, that is, the sea-horse, may enable containment of stimuli (1437) (1877).

          The amygdala detects an unsafe outside world (102) (1054) (1189) (103) (896) (2058) (2220) (2570) (2735) and reacts instinctively, for example with fight, flight (104) (105) or frozen immobility (1190) (471). The amygdala can transmit to the hippocampus directly (1511), and to the inner side of the frontal lobe of the cerebral hemisphere, both directly (878) (1728), and through the thalamus (76) (1867), and its responses can be controlled by the inner side of the frontal lobe of the cerebral hemisphere directly (106) (1835) (2133), through the uncinate fasciculus (1987). The unsafe outside world may be detected through another organism (558), possibly through eye movements (1200) (1528). The amygdala modulates appetitive responses (1082) (1522).
          The central nucleus of the amygdala is old, in evolutionary terms (438), and it delivers generalised, instinctive, unconditioned, responses, which can, in turn, be conditioned (1520) (1514) (1750). The medial nucleus mediates olfaction (536) (471) (2865), and sexual responses (1401) (2073) (2865). The basolateral nuclear complex has evolved more recently (438) (2808), and it is responsive to auditory (1530) (1535) and visual (1529) stimuli, which can be conditioned, perhaps through orthogonality (903). Stress has been reported to produce enduring neuronal changes in the basolateral nucleus of the amygdala, compared with the hippocampus (1544).
          The amygdala requires distinction from its surrounding cortex (1018) (1462) (1019) (1592) (1839) (2150).
          The amygdala and the substantia innominata have been separated (689) and combined (773) in the concept of the extended amygdala (488) (1525) (1491) (2247). A central extended amygdala has been described (1129).
          The potential to extinguish fear memories in anxiety states, including post-traumatic stress disorder, has a theoretical basis in the circuitry of the frontal lobe, the uncinate fasciculus, the amygdala (913), and the basal ganglia (1772), but, in practice, extinction requires the clearest possible distinction between anxiety (2376) (1773) and the arousal of heightened personal identity, and often necessitates the involvement of family members in the treatment plan (2459).
          The phylogeny of the amygdala has been studied in amphibians (1196), and also in goldfish (1197), the latter as part of a contrast with hippocampal phylogeny.

          The nerve cells of the stria terminalis (593) (335) (1856) (2525) detect an unsafe outside world (107), show consistent sex differences (734), and respond to the sex hormones (108) (109) (2073), so that this structure is probably instrumental in orchestration of firstly the inverse relationship between sex and aggressiveness, which relationship has been studied in fish (517) (516), wasps (682), birds (321) (110) (2186), rats (111), prairie voles (1983), and humans (847), and secondly the inverse relationship between parenting and predation (2625).
          Comparison of, say, references (593) (335) (1856) and (2525), conveys a lack of agreement about the nuclear structure of the stria terminalis.
          The stria terminalis and the amygdala have been contrasted (2546).

     Bodily and visceral responses can be conditional upon the responses of others. An example of how a circuit is made between an infant and its mother is in the use of lachrymosity as a signal and as an aid to feeding. Crocodiles shed tears so as to lubricate (116) (1097) and sterilise (1096) their food. The brain cells that activate the lacrimal glands are much closer to the brain cells that activate the salivary glands than they are to the brain cells that activate the eyes (F, figure 224) (1098) (1099) (1100) (609). Hungry human infants signal visceral emptiness through lachrymosity (117) (1102), which then lubricates the act of feeding and feeds the feeder, and which feeds the infant itself if the necessary food does not materialise. Silent, as distinct from noisy, lachrymosity will have protected our cave-dwelling ancestors from predation (498) (118), presumably through parental conditioning (1563), so that there is an evolutionary difference between lachrymosity and crying (1199). An example of how a circuit is made between two adults is when they signal sexual readiness through lachrymosity, which then lubricates the sexual activity: the lacrimal glands are influenced by the sex hormones. The hypothalami control the sequences of hunger, lachrymosity and then feeding, and sexual arousal, lachrymosity and then copulation through the sphenopalatine (pterygopalatine) ganglia. Signals may also be transmitted through odours, as in flies (584) (671) (1922), moths (1156) (668), crickets (1990), beetles (1623), mice (119) (589) (1719), hamsters (537), elephants (346), and humans (120) (515) (793) (794) (795) (777) (1844).   [Back to Pheromones if required.]


     The hypothalami, the substantiae innominatae, the hippocampi, the amygdalae and the striae terminales, in conjunction with the brainstem, the basal ganglia and the inner sides of the cerebral hemispheres, represent the instinctual brain of lower animals (112) (329) (1608) (2244), while the outer sides of the cerebral hemispheres represent the advanced brain of higher animals (286) (1790) (2796) (2848). The hypothalami and the thalami are pivotal in the connecting circuitry (8) (1458a) (1458b) (2154). In an adult human, too much activity in the instinctual brain relative to the advanced brain results in anxiety and irritability, which is another meaning of stress. An example of this is getting out of bed on the wrong side, which really means that responses are not yet being orchestrated by the advanced brain through the thalami, but are coming from the instinctual brain without passing through the thalami. This illustrates the controlled, inhibitory nature of the advanced brain and the spontaneous, excitatory nature of the instinctual brain. Too much activity in the advanced brain relative to the instinctual brain may result in the inhibition of normal responses, such as urination (502) (503) (504) (505). The rate of increase of activity in the instinctual brain may matter as much, if not more, than the absolute level of activity (993). The whole brain has been shown to be as good a predictor of cognitive ability as the advanced brain alone (2040). Damage to the advanced brain may disinhibit the instinctual brain (1081).
     Damage to the instinctual brain disinhibits successively lower levels, so that, for example, mesocortical damage disinhibits subcortical structures (1084). Stress has been followed by structural changes in brain cells (1086) (2258) (2282) (2316) (2398).

     There is diurnal variation in the degree to which the instinctual brain is distributed to the advanced brain, being least in the morning. This is why a seriously depressed patient feels worse in the morning, because his or her instinctual brain has been depleted to the degree that the usual diurnal variation has become intrusive.

     The hormones orchestrated by the hypothalami consign females to lunar variations in the degree to which the instinctual brain is distributed to the advanced brain (264) (284), and thus in the degree of connectedness with the world. When distribution is low, the instinctual brain of the female is more likely to seek increased connectedness with the outside world through the advanced brain of others.
     Hormonal discontinuity is likely to render females more vulnerable to some forms of stress than males, and less vulnerable to other forms of stress than males (1087), the latter because females acquire memories of stress that equip them to cope better. Hormonal discontinuity should be a controlled variable in studies of differences between the sexes (1569) (1845).
     Timed activities and targets are a consequent male response to notional sexual equality.
     Nowadays, disinhibited mobile telephone conversations enable the instinctual brain of a solitary, bleary-eyed human to provoke audible and visible peer responses (M), which then activate his or her sensory thalami. This is an example of regressed human behaviour, which is addressed in more detail in figures seven and eight, and in the related text. From a network perspective, the crucial elements are the induction of a circuit from the instigator to the bystander and back again, and the insight that the part of the instigator's brain that receives the response is not the same part that produced the stimulus. Thus, the purpose of the mobile telephone is not necessarily the transfer of information between two individuals (2005).
     The comparative inability of related, as distinct from unrelated, humans to activate one another's brains is a risk factor for mental illness, and is a major reason for the evolutionary stability of "nonkin" social groups (317). This may be a variant of reduced vigour due to genetic relatedness (578) (579).

      Responses from the advanced brain that pass through the thalami, that is intra-thalamic responses, are orchestrated, planned and measured, and thus carry the connotation of premeditation. (You engaged the gears and set off, so that you were responsible for the journey undertaken.) Responses from the instinctual brain that do not pass through the thalami, that is extra-thalamic responses, are spontaneous, unplanned and unrestrained, like reflexes, and thus do not carry the connotation of premeditation. (You swerved to avoid a lorry.) Thus there is an anatomical basis for criminal responsibility, and this may have physiological correlates (2644).

     The relationship between the advanced brain and the instinctual brain can be remade each day, conditional upon the experiences of the day (1243), such as who we meet, and the activities that we pursue (2193), and this variability has been referred to as plasticity (732), for which there is a chemical basis in hormones (1940) and in acetylcholine (113) (1548), and a physical basis in neuronal spines (1011) (1062), which have been shown to appear (1012) and stabilise (1014) in response to sensory input. Some degree of functional stability, and thus, arguably, of lack of plasticity, is likely in sensory neurones (1013), and perhaps moreso in motor neurones (1006). Plasticity probably varies with age, with age at first reproduction, with gender, and with experience. Plasticity probably increases partner choice. Hallucinations are likely to reflect relative lack of plasticity, while delusions are likely to reflect relative lack of stability.

     In scientific literature, the responses of the controlled, inhibitory, advanced brain may be referred to as "top-down", and the responses of the spontaneous, excitatory, instinctual brain may be referred to as "bottom-up" (114) (115) (511) (614), which conceptual language may reflect the distinctive nature of the scientific brain, and which may seem simplistic to some, for example artists (P, pages 162-164) (2118). Not surprisingly, therefore, the distinction between "top-down" and "bottom-up" has resulted in complexities, because although the distinction has immediate, intuitive meaning, it is anatomically loose, and has meant different things to different people (1494) (1316) (1916) (1134) (1346) (1349) (1607) (2223) (2215) (1927) (2093) (2280) (2416) (2456) (2553) (2675) (2691) (2698) (2717) (2817) (2902) (2904). In The Evolution of Mental Health, the distinction is a vector, "top-down" from the neocortex through the increasingly instinctual mesocortex, allocortex and brainstem, and "bottom-up" from the brainstem through the decreasingly instinctual, allocortex, mesocortex and neocortex (2748).
     To what degree is a conditioned response "top-down" or "bottom-up" (2644)?
     "Hardwired" may mean "bottom-up" activation with little or no potential for "top-down" inhibition, for example instinctual responses.
     Adolescence may include some disproportion between "bottom-up" and "top-down" (1017).

     Aging brings a shift from "bottom-up" to "top-down" (857) (858) (996).
     Anatomical localisation of "top-down" versus "bottom-up" activity has resulted in some pervasive animal experimentation (820), and this writer's view is that the advent of neuroimages should raise the threshold for animal experimentation. Now that we can observe humans directly, the case for inference from animals is weakened, particularly as the inference may be incorrect due to differences between species, not to say between genera, families, and orders.
     The distinction between "top-down" and "bottom-up" can be taken to an extreme, dualist position, when a disorder is seen as either organic, due to disease in the "bottom-up" body, or psychogenic, that is, generated in the "top-down" brain: this has led to surgical interventions, without full exploration of the interaction between the body and the brain (1399) (1408) (1409) (1400) (392) (1318) (2545). If the external urethral sphincter is overactive, then try to relax it with formal distraction and relaxation, before resorting to the invasive insertion of a stimulating lead through the third sacral foramen (504). Observe the effects of formal distraction and relaxation with neuroimages, mindful of the possibility that there may be differences between individual patients that require different emphases on different parts of the circuitry between the body and the brain. Less extreme, but still dualist, is the simplistic question of whether psychological factors or cortical processing modify spinal mechanisms (1315).
     "Top-down" in excess of "bottom-up" is the basis of paranoid misperceptions, when one experiences an inhibited part of oneself as another person through one's own eyes and ears. The inhibition is of subcortical activity by cortical activity, which exaggerates the degree to which one's responses to external stimuli appear to come from those stimuli rather than from ourselves. What is actually an apperception is experienced as a perception. There is a reduction of the corollary discharge that normally signals ownership. This may be due to fatigue, when one's customary level of "bottom-up"activity is depleted relative to one's customary level of "top-down" activity. Irritability may ensue, and the experience lasts for a few hours until rest has been taken. "Top-down" in excess of "bottom-up" that endures for days, weeks or longer is one of the major causes of a reduction in mental health in previously balanced adults. There is "top-down" inhibition of a "bottom-up" anxiety which one wishes to avoid, the nature of which is often revealed when what one purports to see as a problem in other people is actually the very problem about which one feels anxious. One's degree of reluctance to review these possibilities independently is then a measure of the degree to which one's mental health has diminished.
     "Bottom-up" in excess of "top-down" results in a range of experiences, from excitement through anxiety to mania.
     So-called obsessional checking is evidence of attempted "top-down" reassurance in the absence of "bottom-up" introspective knowledge.
     The thespian profession illustrates that plasticity can be acheived in a territory, and that the ability to be plastic can be learned. Acting outside the thespian profession is extremely common, in that humans dissemble and dissimulate so as to conceal their true feelings, thereby to survive in a habitat or in a territory where they feel that the expression of those true feelings would result in extrusion, which, for children, would mean abandonment. The verisimilitude of acting depends on the degree to which the responses can be made to appear "bottom-up" when they are, in fact, "top-down" as evidenced by response latency, and this may depend ultimately on varied formative experiences that develop the ability to mobilise nucleic acids and thus proteins quickly in response to stimuli, and afford a wide range of nucleic acids and thus proteins that have been developed to a degree already (2361).

          The brainstem: the midbrain.

     The top part of the brainstem is the midbrain, which is situated behind the hypothalamus, below the thalamus and in front of the cerebellum. Like the rest of the brainstem, the midbrain has symmetrical right and left parts.

     The midbrain receives auditory (396) (397) (797) (398) (399) (450) and visual (400) (403) (401) (402) (970) (2300) (2307) (2699) (2723) stimuli, and may produce preparatory motor, also called premotor, and motor, responses (121) (1697) (2759). The preparatory motor responses may enter the reverberant system of potential motor responses through the substantia nigra (122) (1313) (453). The same auditory and visual stimuli that enter the midbrain may be transmitted to the thalamus (1763) and also to the cerebral hemisphere (473), where auditory stimuli enter the temporal lobe and visual stimuli enter the occipital lobe (123) (404). Auditory and visual stimuli may also enter the frontal lobe (979) (2594), such that they can reverberate (1148) (1108) (1109) (2025). Preparatory motor and motor responses may be engendered (1715) (2594). The preparatory motor responses may enter the reverberant system of potential motor responses afforded by the basal ganglia. Responses to auditory and visual stimuli that have passed through the thalamus occur after the responses to midbrain stimulation (587) because of the greater number of nerve gaps that have to be traversed. The reverberant system of potential motor responses can thus come to contain both immediate and delayed responses to the same auditory and visual stimuli (446) (447). The immediate responses are more personal and instinctive, whereas the delayed reponses are based more on perception of the outside world.

     Sensory integration occurs in the midbrain (2238). Sensory to motor transformation occurs in the midbrain (1472) (2425) (2507) (2577). Auditory stimuli have been shown to facilitate preparatory motor and motor visual responses (1143). Auditory and visual stimuli may be superadditive, additive, or subadditive (1144) (2057). Midbrain circuits can be conditioned (1176).

     The circuitries of the midbrain and of the thalamus have been contrasted (123) (1145a) (1145b) (1147) (2305).

     Insofar as the eyes influence each other (441) it is likely that the circuitry is in the midbrain (401) (1866), so that it is as reflex as possible.
     One side of the midbrain may compensate for underactivity in the other side of the brain (951).

     Another meaning of stress is that the immediate and delayed responses to the same auditory and visual stimuli contradict each other, as in: "Look" and "Don't look" (1947). A sinister implication is that if the contradiction becomes habitual, it may feel like a split in the brain. The same sinister import accompanies any incongruity between auditory and visual stimuli (124).

     The compactness of the brainstem necessitates convergence, of both sensory stimuli and motor responses. Thus, seasonal variations in arthritic pain may occur partly because temperature changes compete with the established degree of pain sensation for transmission through the brainstem. Electrical stimulators may relieve pain through competitive transmission (823) (1045) (824), and the same mechanism may contribute to "counter-irritants". Conscious pain control has been shown to correlate with brainstem activation (849). The theatrical double-take is consistent with parallel motor responses that "race" (563). Motor responses are particularly condensed and focused in the cells around the central fluid canal of the midbrain, called the periaqueductal gray (2074) (288) (501), where small changes in anatomical location result in large changes in behaviour (489) (490), illustated by maternal responses (108) (564).

     There are nerves that pass from the auditory brain to the ear (173), from the visual brain to the eye (174), from the tactile brain to the ear (619) and to the spinal cord (1533) (2321), and from the olfactory brain to the olfactory bulb, which receives the nerves from the nose (268) (1403). These centrifugal nerves may enable the reverberation of sensory stimuli within the sensory nerve circuits (455), so that the stimuli are contained within a buffer, until transmission is possible. Dopamine may be participative (760) (655) (1830).

          The brainstem: general structure.

     The pons forms a bridge between the two hemispheres of the cerebellum (125) and is below the midbrain and above the medulla oblongata, which is above the spinal cord. The pons and the medulla oblongata include vital centres (1412) (1808); (1487) (126) (2154) (2657)(419) (142b) (1326) (392) (2694) (2702) (2870), and these are contained in segments common to all vertebrates (609).
     The vital centres include the nerves to the larynx (2074) (2294), which organ is a source of responses in the form of pulsations of the frequency and of the amplitude of sounds (P, page 33 and page 43) (2176) (2329) (2600) (2682) (2784). The larynx may convey greater reliability of responses than the face (R, page 273) (2861), and than gestures (2006).
     The midbrain and the pons contain the nerves to the eyes, which may convey greater reliability of responses than the face (2638).

     The entire brainstem, inclusive of the midbrain, is arranged in columns, with three on each side.

     The outer column includes nerves that contain noradrenaline (127) (546), that are stimulated by the outside world (128) and that are particularly active in states of arousal (838), during which states they enable motor responses without loss of vigilance (129) (130), and actually improve motor performance (131) (1631) (888).

     The middle column includes a diffuse reticular network of nerves that facilitates the transmission of both sensory and visceral stimuli (1402) (871) (1320) (2656), and that prepares muscles for motor responses (132) (133) (1488) (1787), with rapidity (1319) (699) (247), and control (2529) (2908).

Figure five

Actual motor responses seem to decrease the level of arousal (520) (K) (592) (1620), which may contribute to the beneficial effects of humour on performance (1673), and which needs to be included in analyses of punishment (80) (2130) (2330) (2357) (2595) (2704) (2755). Exercise may enable the lowering of arousal before it acquires negative content. The diffuse reticular network activates each hippocampus (134) (1427a) (1427b) wherein sensory stimuli can reverberate and evoke memories that can, in turn, reverberate. The diffuse reticular network permeates the entire brain, and is especially concentrated around the thalamus as the reticular nucleus, which is paramount in the orchestration of sensory, motor and visceral activities (62) (2466). The diffuse reticular network has been related to measures of personality, and these have been studied using neuroimages (1028).

     Professional atheletes and martial artists are skilled in the inhibition of marginal movements, with consequent accumulation of arousal, until the critical moment, when one movement set is deployed.
     The diffuse reticular network is phylogenetically old (331) (332), and is thus a likely anatomical basis for responses that are described loosely in the literature as "hardwired" (326) (465), which really means instinctual. The diffuse reticular network should be central to any explanation of emotion (1657).
     The diffuse reticular network is central to consciousness. The diffuse reticular network is distributed to the outer side of the brain, which represents the outside world, and also to the inner side of the brain, which represents the individual. Consciousness is mediated through activation of the outer diffuse reticular network, self-consciousness is mediated by activation of the inner diffuse reticular network, while one form of stress entails excessive activation of the inner diffuse reticular network relative to the outer diffuse reticular network, remedied by transfer of activation from the inner diffuse reticular network to the outer diffuse reticular network, for example by motor responses, or through reflection. One of the reasons why women live longer than men is through their ability to relieve stress by the transfer of activation from the inner diffuse reticular network to the outer diffuse reticular network through the motor response of talk (2132). The success of the religious confessional may reflect the same circuitry.
     The state of readiness afforded by the diffuse reticular network is consistent with a default mode (408) (2878), such that focus brings a redistribution of generalised arousal, with some areas of increased arousal and some areas of decreased arousal, perhaps orchestrated by the zona incerta (58) (71) (986) (2297), and by the reticular thalamic nucleus (62) (748) (2295), which is under the control of the cerebral cortex (1242) (1172).

     A further meaning of stress is that the diffuse reticular network has become overloaded by too much sensory stimulation and too many potential, as distinct from actual, motor responses. To chill out is to recognise this, to disengage from the sensory stimulation of the outside world, to choose some of the potential motor responses and then to implement them.

     Help is nearby, because the inner column of the brainstem includes nerves that contain serotonin, which slow responses (135), inhibit painful stimuli (842), modulate sensory stimuli (887) (2182), reduce anxiety and stress (841), inhibit the diffuse reticular network (215) and control input into the hippocampi (134) (494). All of these functions are consistent with disengagement from the outside world. Relatedly, these cells help to maintain body temperature in spite of thermal changes in the outside world (458) (499), and they also mediate visceral responses (1920).

     It is likely that the columns of the brainstem participate in a basic rest activity cycle (136), with oscillations every few hours, to ensure balanced expression of each mode represented by each pair of columns. Loss of balanced expression may result in symptoms of stress, such as muscular tension, headache, and nausea. Simultaneous expression of all columns reduces stress (538).

     Loss of balanced expression may be due to the absence of another human to provide a focus for personal and visceral activities, which, consequently, reverberate intrusively. The human imposition of an hebdomadal cycle may be of considerable significance.

     The prolonged noradrenaline activity of anxiety may cause headache because the sustained increase in muscle tone causes vasoconstriction (137) (1030), local lactic acidosis (612), and thus cramp in the head muscles (606). Also, if either eye gets too dry, it sets off a lacrimal (138) (483) (484) and vascular (486) (1041) (485) (1413) (487) reflex that is protectively painful. It is well known that anxiety causes a dry mouth, but less so that anxiety causes dry eyes. Lack of habituation between attacks of migraine (1042) (1043) is consistent with anxiety, as is variable delivery of oxygen to the brain (1056) (1776) (1961) consequent upon hyperventilation, and the beneficial effect of anxiolytic drugs such as propranolol (1044). From an evolutionary perspective, moisture on the window of the mind works against the distant vision of vigilance because, in smaller quantities, the refractive activity of the moisture moves the visual focal point towards the eye, while in larger quantities, it simply blurs vision. One eye may be affected by dryness before the other because of local drainage factors, such as the vertical angle of the head. Sufferers from migraine and other headaches could carry a bottle of their own tears, and use these as eye drops to keep their eyes moist during stressful times, signalled by dryness of the eyes (2887), or of the mouth.
     The nitrergic circuitry between neurones (673) and blood vessels (1192) may have relevance in migraine.

     There are nerves that contain choline and dopamine distributed through the brainstem (1547); (784) (785) (1625) (1917) (2168) (2024), and these may be associated with arousal (1802) (2400) (2657), but movement may have been a complication in at least one exposition (780).

          The spinal cord: premotor activity.

     Sensory stimuli reach the spinal cord in nerves from muscles (2227) (2020) and from tendons (141) (2228), as well as from skin (568) and from joints (G, page 57).

     Motor responses may be kept on hold until they are needed (715) (2248), which is likely to be advantageous in the implied states of readiness of tone and of movement. This premotor activity could be orchestrated by the frontal lobes (978) (1174) and could pass through the diffuse reticular network (595), to the brainstem (631) (632) (568) (1325) and spinal cord (633a) (633b) (139) to continue as the sequence of activation of gamma efferent neurones, shortened muscle spindles, activation of 1A afferent neurones, and then inhibition at the synapse between the 1A afferent neurones and alpha motor neurones (140). Other sensory stimuli from muscles could be kept on hold in parallel (568).

     Inhibition of the inhibition at the synapse between the 1A afferent neurones and alpha motor neurones would convert premotor activity into motor responses. This model is consistent with spatially parallel processes (142a), and with temporally early and late inhibition (142c). The subsequent muscle contraction would be sustained only if there was inhibition of 1B afferent neurones, and thus of the tendon reflex (141) (143), and gain could be exercised through variation of the recurrent inhibition afforded by Renshaw cells (569).

     The distribution of activation, and of inhibition of inhibition, of alpha motor neurones between agonist and antagonist muscles, would determine the degree to which the outcome was a change in tone or a movement.

     The appearance of drug-induced parkinsonism is of reduced premotor activity. Indeed, the lesser likelihood and longer latency of movement may be useful.

     The substantia nigra pars compacta is affected in Parkinson's disease, and an implication is that, normally, this structure delivers premotor activity to the spinal cord, perhaps through the activation of gamma efferent neurones. Given that premotor activity requires simultaneous activation and inhibition, and given the unlikelihood that one anatomical structure delivers these opposite functions simultaneously, it is reasonable to suppose that other anatomical structures are required for such premotor activity. The subthalamic nucleus (1471) (1198) (145) (442) (1091) (2104) is at the same level as the substantia nigra pars compacta, and when it is diseased, abnormal limb movements result, consistent with loss of inhibition of alpha motor neurones. This loss of inhibition could then release 1A afferent activation. The substantia nigra pars reticulata may have a similar inhibitory role in the brainstem (146) (147) (831), perhaps in relation to eye movements (1478) (1290) (2310), as distinct from limb movements (1479).
     Existent knowledge of circuitry suggests that the substantia nigra pars compacta delivers activation to brainstem and to the spinal cord through the descending pathways of the substantia nigra pars reticulata and of the subthalamic nucleus, rather than through descending pathways of its own, which have not been identified. In other words, neurones from the substantia nigra pars reticulata (1524) and from the subthalamic nucleus (1765), to the brainstem and to the spinal cord are the final common pathways along which the inhibitory activity of those two structures is modulated by activations from the substantia nigra pars compacta, perhaps through excitatory dendrites (153).

     The globus pallidus is another inhibitory structure (148), and it distributes neurones both to the thalamus and to the brainstem (149) (150). The division of the globus pallidus into an inner part and an outer part may reflect its role as a distributor of muscle tone that enables movement but does not disable posture (151) (1417), for example through a firing-frequency dependent mechanism (152) (2657), acting on differential time windows (265) (997): the sudden-onset trains of > 90 Hz might occur in the larger time window of 400 ms in the outer part of the globus pallidus to enable movement, while the slowly ramped frequencies of 40-60 Hz might operate in the smaller time window of 60 ms in the inner part of the globus pallidus, to maintain tone. Erect posture may have been a major evolutionary impetus for the integration of the substantia nigra and of the subthalamic nucleus with the caudate nucleus, the putamen, and the globus pallidus.
     Neurosurgical perspectives do not give enough emphasis to the systematic examination of tone, as distinct from movement, nor to the comparison of isometric and isotonic contraction (1553) (1554) (2061), although there are exceptions (2290) (1765).

     Normally, premotor activation by the substantia nigra pars compacta is augmented with activation from the caudate nucleus and the putamen, which are driven in turn by perceptions and by memories. Parallel inhibition is delivered through the subthalamic nucleus (573), the substantia nigra pars reticulata (153) and the globus pallidus, to maintain the premotor, as distinct from motor, emphasis. Thus, activation drives inhibition to control activation, for example through striopallidal neurones (51). The caudate nucleus and the putamen are affected in Parkinson's disease (154).

     Premotor activity would become motor activity because of a change in the balance between activation that is inhibited, and the inhibition of that inhibition, which inhibition may require activation (2091). Activation could be varied by the substantia nigra pars compacta, the caudate nucleus and the putamen through the chemical dopamine. Inhibition could be varied by the subthalamic nucleus, the substantia nigra pars reticulata and the globus pallidus through the chemical gamma-amino butyric acid (GABA). Local GABA circuitry has been demonstrated in the substantia nigra pars compacta (1484) (1485), and this would enable inhibitory refinement of its predominantly excitatory circuitry.
     Distinct D1 and D2 receptors (1092) (1897) (2750), different forms of D2 (1202), distinct GABA(A) and GABA(B) receptors (1474) (1094) (997) (2461), a capacity for GABA to activate as well as to inhibit, dependent on time (265) and place (439), the activation of inhibition of GABA (2517), and additional receptors to a fast inhibitor, glycine (1981), would give flexibility in the parallel orchestration of movement and posture. Each of these chemical forms in the brain would have an anatomical correlate in the spinal cord, so that, for example, monosynaptic excitation and disynaptic inhibition in the brain would produce a discrete movement in the spinal cord (1203).
     Studies of the distribution of dopamine in human volunteers should include estimates of movement and of tone (2434).

     Replacement of GABA has been attempted by "subthalamic gene therapy" (2263).

     Individual dopamine neurones are picked out by the thalamus, and by the cerebral cortex using the chemical glutamic acid, and are combined by neurones that contain acetylcholine into functional units (1628) (155) (1368) (1827) (2635) that drive muscle groups in response to perceptions (1481) (156) (534) (1626) and to memories (309) (2555). If dopamine is lost or inhibited, then groups of neurones are activated in blunderbuss fashion (615), which, in the spinal cord, results in movement when a posture is required (tremor) and posture when a movement is required (rigidity) (157).

     For the premotor activity of the basal ganglia circuitry to be realised as purposeful motor activity, it would require orchestration (1449) (2245), to be integrated with those circuits of the thalamus (1248) (1256) (159) (1968), the cerebellum (1300) and the cerebral cortex (158) (556) that also drive alpha motor neurones, but through different pathways, which requirement is particularly evident in sports injuries, when agonists and antagonists have contracted simultaneously during movement, resulting in pulled muscles. Parallel pathways from the frontal lobes may facilitate coordination of eye movements and of limb movements (1480).

     Damage to the thalamus and to the basal ganglia may result in spatial neglect (1501) (1118), which may impair premotor activity.

     Visceral muscles, as distinct from limb and trunk muscles, show premotor activity (1411) (391). The different types of muscle may be controlled by different chemicals (599).

     Human organisms who are unsure about which premotor responses to choose have been known to seek direction through the feedback from their own motor demonstrativeness, like the lady who protested too much.

     Like the motor activity it precedes, premotor activity can induce a mental set, a notable feature of which is a raised threshold to perceptions other than those that generated the premotor activity: this affords focus, at the expense of vigilance. In conversation, there may be a consequent insensitivity to cues that other people want to speak. Very intense levels of premotor activity can become repetitive, because of the wish to avoid the unpleasant emptiness inherent in a change of mental set, so that there is a driven search for perceptions relevant to the existent mental set, and this is enabled by nerve fibres that descend from the visual (160) and auditory cortices (161) to the midbrain, where new sensory input can be gated.

     The gamma efferent activity mediated through the brainstem and spinal cord contributes to facial, vocal and postural changes, and is thus a correlate of the mental state (2020).

     The existence of premotor activity creates the need to establish that a movement has actually occurred, as distinct from having been about to occur, and this is expressed in corollary discharge (162) (201) (163) (1508) (1715).

     Movement itself is a sensory stimulus that needs to be inhibited as part of premotor control (1276).

     Gravity increases greatly the number of motor responses that need to be kept on hold, in the form of states of readiness of tone. Hence the dramatic change in sleep pattern when the fur seal leaves the sea for land (334).

          Brain cells.

     Nerves are brain cells, also called neurones, while nerve circuits are sequences of brain cells that are separated from one another by gaps which, if bridged chemically, are called synapses (1375), and if bridged electrically are called gap junctions (535), or electrical synapses (1414). Chemical and electrical synapses may coexist within the same neurone pair (2382). Developmentally, gap junctions have been seen to be supplanted by chemical synapses in the cerebral cortex (917). Electrical connections are quicker than chemical connections (1456), but the temporal advantage may result in a spatial disadvantage, in that the varied actions of different chemicals on the cell membrane are unavaliable (539). Electrical connections may support synchrony (1860), whereas chemical connections may mediate asynchrony (1415). Synthesis of chemical connections has been addressed (2428). The average synaptic distance is 15-19 nm (1909). Average synaptic times are a peak of 0.3 ms and a decay over 2-5 ms (1914) (1915).
     The gaps between brain cells place a time limit on how quickly the outside world can be processed by the brain (1832). Our sense of time is probably based on the time taken for a gap to be bridged (604) (2787). Illusions of time may reflect variations within the range of gap time, compared with real time: when the brain works quickly, so that gaps are bridged quickly, then events will appear to slow down, assuming that they continue to occur at a constant rate in real time (605) (2797) (2837). Subjective rhythmicity given to objective events may reflect reverberation through circuits within which the number of gaps has been fixed for a finite period, perhaps by perceptions or by memories or by some combination thereof; such rhythms may be recognisable between organisms through actions (P, pages 146-148). Timed control has activated the language areas of the left cerebral hemisphere (2068). Elapsed time has activated cells in the frontal lobe (2102).
     The gaps between brain cells enable nerve circuits to be made and broken in response to changes in the outside world, which molecular changes have been particularly well studied in olfaction (1253) (1254) (1255a) (1255b). Simple circuits are made through activation and are broken through inhibition, while more complex circuits may be made through inhibition (265) (439) (2452) (2822). Time is given precision through inhibition (1231) (1232) (1244). Gaps can be bridged in both directions (956) (905) (1359). Brain cells may inhibit themselves (2199). Hormones have been reported to modify synaptic activity (1342) (1940).
     Brain cells respond after stimulation has reached a threshold (2360). Stimuli may interact predictably, both above and below threshold (2721).
     Brain cells become refractory after stimulation, to allow chemical recovery, so that the absence of a response to a repeated stimulus may be a passive process (1447) (2380) (2639): the geometry of some brain cells may reflect this constraint (1758). Gaps between brain cells vary with temperature (1794).
     Circuits may be made between brain cells and blood vessels (673) (1192) (1304) (1371) (2355).
     The back of the mind and the front of the mind are not places in the anatomical sense, but are greater and lesser degrees of synaptic inhibition, respectively. This inhibition can be orchestrated by the frontal lobes, which activity is utilised in hypnosis (240). The inhibitory capacity of the brain is evident in the blindness that results to an eye that presents an eccentric image to the brain (2101), referred to as suppression (1149). Visual suppression has been found to be greater in adolescents than in young adults (1135). Repetition suppression has been used as an index of activity (1447) (2380). Consignment of ideas, feelings and images to the back of the mind requires mental effort, so that it is achieved at a cost (2713), and it utilises attentional resources (P, pages 140-141). Models of attention are unlikely to reach consensus (1065) without these considerations. If a psychiatric disturbance reflects the activation of aberrant unconscious memory processes (1376), then the timing of the activation requires explanation (683). "Hardwired" may mean that some activations are difficult to inhibit, for example instinctual responses.
     The more inhibited a personal idea is, and thus the further back in the mind it is, then the more likely it is to appear in the front of the mind as someone else's idea, because whenever the idea is evoked by circumstances, there is a lack of personal repsonses that would give ownership to the idea, and to any associated memories.
     Attempts have been made to identify the neural correlates of beauty (701), which attempts have transcended the cosmetic masquerade perpetrated deathlessly by the escapist media. The beauty of the Mona Lisa may include the depiction of a personal response consigned to the back of the mind, which means that men can be beautiful too. The face and the body may stimulate different parts of the brain of the beholder (2115). Correlations between visual attractiveness and vocal attractiveness have been shown to vary with gender and with facial movement (2343).
     For an historical perspective of the study of nerve cells and of nerve circuits, see reference (1936).

     Each cerebral hemisphere is lined by brain cells that comprise the cerebral cortex and that are arranged in layers, usually six in number (164) (165) (166).
     The brain cells that represent the individual are in circuits that include personal responses, pain and visceral sensation, and these circuits are on the medial side of each cerebral hemisphere, whereas the brain cells that represent the outside world are in circuits on the lateral side of each cerebral hemisphere.
     Brain cells may be generated during adult life (273) (330) (740) (2126) (2524) (2590) (2671) in some parts of the brain (2373) (2714), subject to the effects of mental activity (1422) (1431) (1406) (1423) (1424) (1432), of physical activity (1407) (1580), of a critical period (1901), of age (2211), of stress (955) (933), of sleep (1740), of social structure (2201) (2804), of housing conditions (1581) (2653), of irradiation (2112), of disease (998) (1516) (1783), and of drugs (2389). Cell counts may vary with techniques (2616). The generation of brain cells during adolescence has been shown to be very sensitive to inhibition by alcohol (1998). Generation may be possible through chemical (1010) (1061) (1582) (1688) (1730) and electrical (2018) (2695) stimulation. The sprouting of new connections between brain cells may contribute to epilepsy (2460).
     Within the cerebral cortex, the inner cell layers perceive immediate sensory stimuli (167) and produce immediate motor responses (323), while the outer cell layers evoke past sensory experiences, that is memories (1280) (1040) (1743), which may modulate immediate motor responses (953) (958).
     The immediate sensory stimuli to a particular cortical cell column (945) may reverberate through the laminae of that column in circuitry inclusive of the thalamus (170) (1841) (1965), while memories arrive in the outer layers of that column through the neocortex (169), and through the mesocortex (1468c), subject to attention (1247a) (1247b) (2456). This could be expressed in the electroencephalograph as an initial burst, then a pause, then more sustained activity (966).
     Evoked past responses may feed forward to vary immediate responses (1824), as when a reward is expected to occur (2014). When an expected reward fails to occur, the disparity between immediate sensory stimuli and memories may activate motor responses to remove the disparity (172), for example by foraging (1058). Perceived discrepancy between current body image and remembered body image may drive sexual behaviour, perhaps through variations in testosterone levels (393). Facial metrics (2537), and a small waist-to-hip ratio (1879), remind us of when we were young. Memory minus perception equals action, which translates chemically into acetylcholine (2298) (2304) (2876) (2882) minus adrenaline (2835) equals dopamine (891).
     The placebo effect is likely to include the activation of memories of pain relief by the prospect of pain relief (R, pages 263-264) (171) (2111) (2696), perhaps through the activation of inhibitory circuits driven by the cerebral cortical outer cell layers in response to the perception of analgesics by the cerebral cortical inner cell layers.
     Perception in the inner cell layers is subject to memory in the outer cell layers, that is the eye of the beholder (904) (2302). The impassivity of any seducer and of some film stars is intended to minimise disruption by the inner cell layers of what is active in the outer cell layers.
     The outer cell layers are the mind's eye and the mind's ear (P, page 5, and page 167).
     In conversation, a stressed human sometimes talks about the memories evoked by the other person rather than to the immediate perception of that person, which feels like insensitivity to that other person; this is part of the logic of indirect speech (2333).
     Given that the cellular basis of perception is cells in layers 4 to 6 of the cerebral cortex and the cellular basis of memory is cells in layers 1 to 3 of the cerebral cortex, and given that the subject is represented by the mesocortex on the inner side of both cerebral hemispheres while the object is represented by the neocortex on the outer side of both cerebral hemispheres, the social soliloquy is in fact a dialogue wholly within the brain of the subject, specifically between cells in layers 1 to 3 of the mesocortex on the inner side of both cerebral hemispheres and cells in layers 1 to 3 of the neocortex on the outer side of both cerebral hemispheres. Syntactic rules are not sensitive to this variation, illustrative of their reducibility. [Back to Theories of language or The cerebral hemispheres if required.]

     Insofar as an organism's perception of the world through sensory stimuli is altered by its own brain, for example by its memories, then that experience of the world is called apperception, which carries the implications that different organisms may experience the same world in different ways at the same time (2007) (2189) (2409), and the same organism may experience the same world in different ways at different times (605) (2147). The frequency of a sound is the physical vibration, while the pitch of the same sound is the psychological experience, (P, page 29). Attempts to explain the relationship between sensory stimuli and responses in terms of the sensory stimuli alone, such as Weber's Law and Fechner's Law, have been shown to be approximations at best (1296) (1297) (1123) (1875) (2645) (2744). Prey may avoid predation through disruption of the predator's memories, as distinct from its perceptions (1564). The organism makes adjustments, through the eyes (2078) (2077) (220), through the ears (2075) (2076) (P, pages 63-68, page 277, and page 378), and through the brain (2430) (R, page 289, and pages 291-296) (1298) (1575) (1649) (1777) (1878) (2422) (2722). Thus, an effect of a pure tone of 700 ~ and 80 db on the inner ear has been shown to be the production of subjective overtones, that is overtones with distinct pitch, loudness and harmonic relation to the fundamental, but with no corresponding physical frequency (P, page 65) (2075), perhaps because of amplification by the outer hair cells of the cochlea (2137) (2138) (1345) (1263) (2177) (2013). Tones have been made to disappear through competition (2146). Gaps in perception are filled in by the organism (1267) (476) (2397); (1705) (1863) (1956) (2431). The demonstration of fibres that pass from the hypothalami and from the hippocampi to the retinae, suggests circuitry whereby memories could alter perceptions (647) (1587).
     The occult exists because of lack of introspective knowledge (R, page 172). The containment of anger does feel like something unpleasant inside (854), and this needs to be included in analyses of punishment (80) (2130) (2330) (2357) (2595) (2704) (2755). One's brain is divided into self, inside, and others, outside. A perception of an object or of a person can remove inhibitions, so that something unpleasant inside appears to move from inside to outside. It is this lack of introspective knowledge that gives the occult its extrospective force.
     There are less dramatic, more mundane ways of shifting an unpleasant feeling from inside to outside, that is, from the part of the brain associated with personal responses, to the part of the brain associated with perception of the outside world, especially other people: these include confession, regression, sexual activity, and the ubiquitous, non-intersecting soliloquies of 'buses, corridors, shops, and telephones. Electronic mails (818) (678), mobile telephones (1923) (2005), and a website (2231) have been illustrative.
     A major developmental issue is how parents deal with the responses of their offspring that are unexpected and that reflect the distinctive genetic mix of those offspring. Some members of English society have reacted by trying to have their supposedly aberrant children labelled as "mentally ill" by a psychiatrist, when all the children have been doing is experiencing the same world in different ways to their parents at the same time (588).
     Consistency in the outside world makes it easier for a child to realise how it may vary in its experience of the immediate outside world through its memories.
     Language is subject to apperception, so that particular words mean different things to different people. An example in psychiatric language is "Freudian", an example in neuroscientific language is "limbic" (2139) (2140) (1934), while examples in scientific language are "gene" (1637), "endangered" (1975), "species" (2253) (1941), and "behaviour" (2602).

     The electrical activity of brain cells is cyclical, like alternating current, which means that it is relatively easy to stop at any moment in response to an event in the outside world, because, by its very nature, it is at the zero point on a regular basis. Like the electrical activity of the home, the electrical activity of the brain incurs costs (2605).
     If neurones cycle independently rather than in groups, then at any given moment, at least one of them will be close to discharge and free from interference by the other neurones that are at different points in the cycle (177). The loss of these individual neuronal cycles, and the resultant synchronous discharge of groups of neurones is abnormal, as is seen in Parkinson's disease (178) (2478), dystonia (1166) and experimental parkinsonism (1167).
     The electrical activity of brain cells is detectable in the electroencephalograph (1312) (292), in the electrocorticograph (1862) (2066) (2604) (2619) (2877) (2890), and through intracranial electrodes (2720), as alpha waves (179) (427) (670) (1543) (2436) (2717), beta waves (54) (1542) (1543) (2378) (2772) (2810) (2818), gamma waves (139) (1382) (1542) (1621) (2179) (2284) (2611) (2650) (2773) (2830) (2818) (2882), delta waves (184) (2480) (2720), theta waves (313) (1382) (1388) (1621) (2720) (2743) (2772) (2775) (2882) (2923), slow waves (987) (988), spikes, and spindles (1594), and mu waves (2775), which phenomena have been studied from electrical (314) (1334), clinical (184) (1846) (2286) (2405); (1395) (2287) (2404)(1622) (1770) (2033)(2030) (2031), cellular (1380) (1457) (296), and vascular (1076) (636), perspectives, and, also, in relation to attention (1609) (1927) (2063) (2163) (2187) (2284) (2772), perception (1840) (2556); (2125) (2830); (1311) (2818); (443) (645) (1891) (2443) (2650) (2810), pain (2901), movement (2569) (2701) (2775), working memory (1995) (1707) (1900) (2197) (2198) (2477) (2612) (2773), learning (180) (1258), remembering - both recognition (267) (1175) (1708) (1709) (1710) (2378) and recall (798) (1383) (1594), conflict (2923), sleep (82) (84) (1594), behaviour consequent upon remembering (315), complex natural stimuli (1829), personality (1465) (1541) (2283) (2285) (2496), social performance (2010), and performance in traffic (2163) (2479). Rewards have increased the power of existent brain waves (513) (2651), indicative of the association between focused attention and visceral activity. Brain waves have been shown to be sensitive to modulations of sound waves (674) (2626) (2641). Sensory oscillations have been found in invertebrates, suggestive of evolutionary importance (635). Oscillations have been studied in three dimensions (1377).
     It is unremarkable that the neuronal spikes that generate brain oscillations are to some degree correlated with those oscillations (1955).
     A change in the outside world may be registered by one of a group of brain cells firing out of phase (181) (182) (1405). Different aspects of actuality may be represented by the difference between amplitude and frequency (1605), and, within frequency, between the effects of regular and irregular stimuli (1834), between bursts and spikes of electrical activity (1506) (183) (659) (833) (2256), and also by systematic variations within bursts and within spikes (590) (1606) (2309a) (2309b) (2318). Bursts have been shown to predict behavioural responses (1658) (2009). Burst and tonic response modes have been contrasted in the relays between the thalamus and the cerebral cortex (2531, pages 247-250, and pages 313-314). The timing of electrical activity, as a response, may reflect the number of nerve gaps crossed following the stimulus (1593). The information per spike has been reported to be greater at lower firing rates (1287). Different spike patterns have been observed in males and in females (1205). A change in the body may be coded by a change in rate (643). Different firing patterns have been shown between different cortical areas (866) and between different cortical layers within the same cortical areas (866) (867). Within the motor system, averages may be more instructive than individual spikes (931). Active movement and passive movement have produced different firing patterns (1519).
     The explanatory value of electroencephalographic activity is debatable, as reflected in references (763) and (764).
     Related techniques include electromyography (2294) (2375) (2288) (2403) (2406) (2776) (2781), sonography (2437), acoustic analysis (2481), visual image analysis (2498) (2515), magnetoencephalography (674) (2164) (2475) (2490) (2611) (2626) (2627) (2701) (2770) (2771) (2773) (2774) (2794) (2881), transcranial magnetic stimulation (2354) (2402) (2448) (2769) (2792) (2821) (2823) (2871) (2875) (2879), brainstem stimulation (2544), and transcutaneous electrical stimulation (2497).

          Genes.

     Cells have a nucleus and a cytoplasm, that is a cell body, surrounded by a cell membrane. The interaction between heredity and the environment begins when sensory stimuli cause changes in a cell (1266) (1259) (1441) (1717) (2731); (1253) (1254) (1255a) (1255b) (1718) (1919) (1982) (2037) (2826); (1228) (1873) (2326) (2152) (2319) (2527) (2627) (2630) (2924) (2687) (2747) (2727) (2872) (2844); (1345) (1261) (1262) (1263) (2177) (2013) (1771) (1837) (2110); (1921) (2181) (2184) (2334); (1803) (1804) (1757) (2588), which changes may be transmitted to neighbouring cells. Within a nerve circuit of brain cells, chemicals released by one brain cell cross the synapse and cause the shape of the cell membrane of an adjacent brain cell to alter (1384) (660) (591) (770), which, in turn, activates changes in chemicals in the cytoplasm of that adjacent brain cell. These cytoplasmic chemicals may include proteins, (667) phosphates, calcium and fats, and the changes in them are transmitted to the cell nucleus. Within minutes of a sensory stimulus (175), the deoxyribonucleic acid [DNA] in the genes of the cell nucleus sends ribonucleic acid [RNA] (1712) into the cytoplasm to make new protein (1713) in response to the new sensory stimulus. For example, a painful stimulus may produce proteins that inhibit pain transmission between brain cells; a sensory experience may induce new memories (176) (1385) (1747).

     Adaptive cellular changes are more likely to occur if the organism is in safe repose, so that an adult human who finds a safe place, activates the serotonin nerves to stop input to the hippocampus and then reflects, will reduce levels of stress.

     Chemical changes in the genes of patients with mental illness may be consequences of the illness, or of its treatment.

     The possession of a particular gene has very little predictive value with respect to any mental illness, and the diagnosis of any mental illness has very little predictive value with respect to the possession of a particular gene.

     Our genes limit our instincts. Our genes limit our potential to inhibit our instincts. Our genes do not limit the potential of the adults who rear us to influence our instincts and our potential to inhibit our instincts. Hence the limited predictive value of genes in relation to mental illness (860) (1929) (1930).

     We inherit through our genes an array of potential responses, but these require to be developed for us by our family (2129), even if they do not use those responses themselves.

     Twin concordance may reflect placental overlap.

     Genetic therapy requires a risk assesment, and sustained follow-up over decades.

     Genetic chemistry is very intricate (1637).

          Cell nuclei are so small, that the process of study of nuclear DNA may influence the findings (417).
          Different cell nuclei in the same organism may have different configurations of DNA (389) (2673).

          The chemicals orchestrated by sequences of nuclear DNA known as genes are RNA (379) and then cytoplasmic protein (325) (378) (650) (2427).
          Some parts of the sequences of nuclear DNA known as genes do not orchestrate RNA and then cytoplasmic protein (324) (1716) (1722) (2084).
          The parts of the sequences of nuclear DNA known as genes that do not orchestrate RNA and then cytoplasmic protein, are called introns in reference (324), but one such part is called an exon in reference (1655).
          Some parts of the sequences of nuclear DNA known as genes that do not orchestrate RNA and then cytoplasmic protein, may interact with the nuclear DNA that does orchestrate RNA, and with RNA (1110).
          Identical nuclear DNA sequences known as genes may produce different chemicals at different times (656).
          The sequences of nuclear DNA known as genes can be induced to produce different chemicals at different times (256) (627) (1369).
          The same sequences of nuclear DNA known as genes may produce different chemicals at the same time (684) (1350).
          Some sequences of DNA known as genes may be cryptic within the cell nucleus (333), perhaps kept in reserve.
          Some sequences of DNA known as genes are duplicated within the cell nucleus (426) (768) (799) (1721) (1741), perhaps kept in reserve in the event of damage, and thus of the need for repair (1974).
          The sequences of nuclear DNA known as genes have been classed as repetitive and non-repetitive (2798).
          The duplication of sequences of nuclear DNA known as genes within the cell nucleus has been associated with disease (2127).
          The sequences of nuclear DNA known as genes may recombine (703) (735), perhaps to produce robustness (788), or to encode a new memory (827) (1268). The causal relationship with mating is likely to be instructive (1555).
          Recombinations and mutations are both produced by the crossing over of sequences of nuclear DNA known as genes, between chromosomes, in germ cells (788) (1924).
          The capacity for mutation enables adaptation to environmental change (1993) (2858).
          The sequences of nuclear DNA known as chromosomes may be inhibited by the sequences of nuclear DNA known as chromosomes (281) (282) (283) (716) (717).
          One of the X chromosomes may be inactive (1871) (2084).
          Some sequences of nuclear DNA on the inhibited X chromosome escape inhibition (1003).
          The sequences of nuclear DNA known as chromosomes may be remodelled (1655) (385).
          The sequences of nuclear DNA known as genes may be inhibited by the sequences of nuclear DNA known as genes (333) (680) (1642) (2011).
          The sequences of nuclear DNA known as genes may add to the sequences of nuclear DNA known as genes (688) (860) (1642) (2011).
          The relationships between the sequences of nuclear DNA known as genes may vary over time (324) (692) (1677), and in place (1677).
          The sequences of nuclear DNA known as genes may be inhibited by RNA (789) (915).
          RNA may be inhibited by short RNA (1064) (1439).
          RNA may be inhibited by microRNA (1643).
          RNA induces retraction of synapses and of dendritic spines (1193).
          Repression may have molecular correlates (1154) (1517) (1591) (2617), as may suppression (2618). However, the introduction of the words repression and suppression, with their emotional connotations, rather than the use of the word inhibition, with its chemical denotations, requires molecular justification, lest we fail to learn from psychiatry (1591) (A).
          The sequences of nuclear DNA known as genes that are inherited from each parent may be expressed differentially (281) (282) (283) (723), perhaps in response to differential stimulation by each parent.
          The sequences of nuclear DNA known as genes may be inherited atavistically, from grandparents but not from parents, perhaps through ancestral RNA (1659).
          The sequences of nuclear DNA known as genes may be altered atavistically, for example, through a grandmother's diet (1734).
          Chemical changes may occur in the cell independent of changes of the sequences of nuclear DNA known as genes (385); some of these changes may be due to variations in RNA (708) (704) (705) (706) (707).
          Chemical changes may occur in the cell independent of the orchestration by sequences of nuclear DNA known as genes of RNA and then of cytoplasmic protein; the time-scale of these chemical changes is 15 to 30 minutes (88), compared with a time-scale of 2 to 4 hours for the orchestration by sequences of nuclear DNA known as genes of RNA and then of cytoplasmic protein (175).
          Chemical changes may be transmitted across generations (225) (1071) (1577), notionally independent of changes of the sequences of nuclear DNA known as genes (386) (810), called epigenetic inheritance (387) (388) (809). There is no epigene (2085), but there is an epigenome (2086), and there are epigenotypes (2087).
          The relationship between synaptic chemicals, on the one hand, and, on the other hand, the orchestration by sequences of nuclear DNA known as genes of RNA and then of cytoplasmic protein, is propositional (175) (942) (176) (1534) (626) (648) (1795) (1847).
          Behavioural changes that require transcription are likely to take longer then behavioural changes that only require translation, which, in turn, will probably take longer than behavioural changes that just require the release of existent protein from a neurone into a synapse. Sleep may be needed for the more complex alterations.
          Cross-sectional findings may be correlates, or consequences, rather than causes (708) (707) (390) (724) (938) (709) (1944) (1665) (1036) (1469) (1742) (1996) (1852) (1885).
          Cross-sectional findings have been used to infer genetic ancestry (2180).
          Changes in the environment are not necessarily followed by chemical changes in sequences of nuclear DNA known as genes (713) (333) (746) (747).
          The sequences of nuclear DNA known as genes may include modules (684).
          The sequences of nuclear DNA known as genes may show oscillations (843).
          The same sequences of nuclear DNA known as genes may be associated with different effects, called pleiotropy (333) (684), and phenotypic polymorphism (1207).
          The same effects may be associated with different sequences of nuclear DNA known as genes, called genetic polymorphism (1208) (2043).
          Different sequences of nuclear DNA known as genes may be adapted equally to a given environment (731).
          The same sequences of nuclear DNA known as genes may be adapted differently to a given environment, and this may slow evolution (2202).
          Too much similarity between neighbouring sequences of nuclear DNA predicts social mobility (317) (578) (579).
          Sequences of DNA may move around the nucleus (378), sometimes through the intermediary activity of RNA (669) (690).
          Sequences of DNA may be present in the cytoplasm (720) (1764).
          Some sequences of DNA present in the cytoplasm of plant cells may transfer into the cell nuclei (1925).
          Some sequences of nuclear DNA known as chromosomes characterise mammals (2050).
          Some sequences of nuclear DNA known as chromosomes, characterise mammals, as distinct from birds, and from reptiles (1735).
          Some sequences of nuclear DNA known as genes characterise mammals, as distinct from birds (726).
          Some sequences of nuclear DNA known as genes have been conserved between fishes and mammals (1761).
          Within the class of mammals, some sequences of nuclear DNA known as genes may have the same (1722) (2128) or different (952) effects.
          The parts of the sequences of nuclear DNA known as genes that do not orchestrate RNA and then cytoplasmic protein have been shown to vary more than the parts of the sequences of nuclear DNA that do orchestrate RNA and then cytoplasmic protein, in one group of mammals compared with another group of mammals (2084).
          Sequences of nuclear DNA known as genes have been compared within the order of primates, with the production of a blueprint (1988), and of drafts (1989).
          Some sequences of nuclear DNA known as genes have been shown to be conserved to a greater degree in the subcortex than in the cerebral cortex, between species, within the order of primates (1733).
          Some diseases may occur because sequences of nuclear DNA known as genes are shared by mammals and microorganisms (1308).
          Genes may be transferred horizontally (1881).
          Some diseases are associated with instability of the sequences of nuclear DNA known as genes (1798).
          The addition of a gene to treat one disease may increase the risk of another disease (806).
          The deletion of a gene to prevent a disease may expose the subject to other diseases.
          The addition or deletion of genes may affect fertility, aging, and, in animals, predation risk (1702).
          Models of gene structure and function are available (168) (786) (826) (834).
          The assignment of fixed probabilities to many genes is simplistic, given the variation that can occur between some genes and the subsequent expression of characteristics (781) (1552).

     For a literate critique, see reference (O).

     Incredulity that genes associated with mental illness, and thus with reduced fertility, should persist across generations (2520), suggests simplistic ideas about genes (1637). Genes exist in a genetic environment (2880). Genes are structured as reciprocal pairs, with one member of each reciprocal pair derived from each parent. The chemical responses of any reciprocal gene depend on the other reciprocal gene, and also on the reciprocal genes of other pairs, and it is this distinctive genetic network that is associated with mental illness and reduced fertility in any individual.
     The relationship between reciprocal genes may vary over time within an individual (2905).
     The relationship between reciprocal genes may be altered by the meiotic chromosomal reconfigurations that precede fertilisation (2607). Arguably, meiosis acts as a circuit-breaker that removes the network inhibitions of reciprocal genes occasioned during the life of the potential parent to date, and thereby makes those reciprocal genes available to offspring in uninhibited form.
     Protein-coding changes may be less important than regulatory changes (2607) (2798) (2819) (2858).

A DETAILED GUIDE TO THE DEVELOPMENT OF MENTAL ILLNESS.

         The frontal lobe.

     The sensory awareness, motor responsiveness and body images of the cerebral hemisphere can be brought into focus by its frontal lobe (185), between modes by orchestration of the thalamus (1172), and within modes by a process of central activation and lateral, or surround inhibition, which also involves the thalamus (1489) (187) (1490) (1221) (1822), and which is present in both the sensory system (186) (188) (1150) (481) (429) (491), and the motor system (189) (837). For tactile stimuli, the distribution of central activation and surround inhibition may depend on whether one hand is used, or whether both hands are used (890).
     Lateral inhibition is only one way in which the brain orchestrates sensory stimuli to produce perceptions (1152) (1153) (2760). The same central and peripheral stimuli are orchestrated by the brain in a different way to produce the perception of movement (675), and in yet another way to negotiate darkness (1121) (220) (992) (1151) (1418) (1858) (1957). Inhibition is used to resolve time (1231) (1232) (1244), as well as space (1732).
     Excessive lateral inhibition has been implicated in developmental disorders (1675).
     A corollary of lateral inhibition has been referred to as relative blindsight (1737).
     Given their lives so far, patients with schizophrenia may prefer the bigger picture (1699).

     The frontal lobe contains brain cells that continue to respond after the stimulus has ceased (1005), to a degree that reflects the duration of the stimulus (2102) (2444). Relatedly, each frontal lobe interacts with its parietal (192) (916) (524a) (524b) (1789) (2065) (2183) (2566) (2591) (2592) (2773) (2824), occipital (191) (872) (1695) and temporal lobes (479) (977) (1695) (1703), to contain not only the sensory stimuli transmitted to those lobes by the thalamus (1902) (2215), but also the memories evoked by those sensory stimuli (2350), even after the stimuli have ended, with retention of the order of the stimuli (2170): this is called working memory (199) (1903) (2027) (2754). In the same way, each frontal lobe assists its basal ganglia (477) (2820), that is the caudate nucleus (2613), the putamen (570) and the globus pallidus, and its midbrain (957) in the production and containment of potential motor responses through dopamine (382) (193) (194) (190) (381), and can stabilise the potential responses from interference by irrelevant stimuli. Potential motor responses include eye movements (911) (1752) (1966). The frontal lobe can also maintain a response after attention has ended to a stimulus that has continued (1331). The cerebellum may be participative (950) (2463).
     It follows that stimuli can occur without responses, that responses can occur without stimuli, and that responses may follow stimuli arbitrarily. Responses may occur because of the need to avoid overload by too many reverberant potential motor responses in the output, motor side of the working memory system. Ethological concepts of releasers (K), and some psychological concepts of stimuli and responses (449), appear simplistic in this context.
     Working memory represents a major challenge to empiricism and phenomenology, where these terms mean taking things at face value (565) (2054).
     The graphical relationship between performance, as ordinate, and reverberation, as abscissa, may be an inverted U (472).
     Working memory has generated its own vocabulary (1332), inclusive of encoding (623) (2778), load (195), maintenance (623) (729) (2778), buffer (624), interference (195) (622) (2612), nonemotional distracters (1616), distractors and interruptors (2612), rule implementation (544), temporal segmentation (1352), domain-general or domain-specific component subsystems (1340), flexible updating (switching) (2026), discrete fixed-capacity (2420), and the oxymoronic non-mnemonic role (521).
     Working memory has been explored during infancy (2512), while the development of working memory between the ages of 8 and 30 has been studied (863) (1696) (2550), as has the adaptation of working memory to aging (1745) (2628).
     Working memory dysfunction is not a core component of schizophrenia (737) (2331) (2442), and it is just as likely that "the pervasive and profound cognitive deficits observed in patients with this illness" contribute substantially to working memory dysfunction, as it is that working memory dysfunction contributes substantially to "the pervasive and profound cognitive deficits observed in patients with this illness." (478). Hallucinations, delusions, and treatment may also contribute substantially to working memory dysfunction in patients with this illness (621).
     "Give me a reminder..." is a regressed attempt to increase one's working memory capacity through someone else. Electronic mails, telephone calls and telephone texts may be used for the same effect.
     In written texts, a "window of attention" of 100 words has been studied (767). Covert attention is likely to be a correlate of working memory (2417).
     Working memory is just that, work, so that it is achieved at a cost (1344).
     Working memory for sensory stimuli is consistent with the greater number of neurones engaged in the internal representation of a stimulus compared with its transduction (1177).
     If a bigger brain means more synapses (1887), then it may confer an advantage in terms of reverberatory capacity, and thus of working memory.
     Working memory applies to sounds as well as to words, (P, page 339).
     The anatomical correlates of verbal working memory and of sentence comprehension have been compared (2067).
     The circuitry of working memory may overlap the circuitry of longer term memory (1046).
     Working memory capacity has been shown to correlate with the rate of motor sequence learning (2597) (2628).
     Working memory has electroencephalographic correlates (1995) (1707) (1900) (2197) (2198) (2477) (2612) (2773).
     With the motor system on hold in cortical layer 5 (acetylcholine) (936), and against the template of consolidated memory (acetylcholine) (424) (425) (1433), working memory (dopamine) (688), (dopamine D1) (193) (941) (dopamine D5) (1368) is stabilised from perceptual (GABA) (193) (2677) and visceral (serotonin) (381) interference, while remaining perceptually aware (noradrenaline) (129), able to activate the motor system (dopamine D2) (761) through cortical layer 5 (382), and responsive to chemical closure (430), all provided that steroid responses have not been affected by stress (848). Spontaneous firing is not necessarily noise (664), it may be consolidated memory.
     A dopamine D1 agonist has been shown to improve working memory in aged monkeys, but not in young adult monkeys (944), perhaps through gain modulation of layer 5 pyramidal neurones (2449). A dopamine D1-D2 agonist had mixed effects in humans (1354), whereas a D2 agonist improved flexible updating (switching) in impulsive humans (2026).
     An association has been demonstrated between impairment of spatial working memory, and neuronal loss in layer 2 of the cingulate cortices, in rats given dexamethasone (919).
     Working memory has been found to improve following brain damage (1882).

     The frontal lobe transforms a potential motor response into an actual motor response (196) (540), through the inhibition of an old motor response made obsolescent by a new sensory stimulus (2825), and then the activation of a new motor response that is relevant to the new sensory stimulus (197) (547). This inhibition of old motor responses in the face of new sensory stimuli is subject to fatigue, so that an old motor response may persist in spite of a change of sensory stimulus, which is called perseveration.

     There are other definitions of perseveration (1241). Brain damage has resulted in sensory persistence, when the tactile sensory stimulus has stopped, but the sensation of touch has continued (1252).

     The frontal lobe may produce a particular mental set, through the activation of the outer cell layers of the cerebral cortex, which evokes a set of memories that the organism then tries to match in the inner cell layers of the cerebral cortex by search of the outside world for the relevant sensory stimuli (839) (1724). The existence of a prior mental set facilitates memory (1928). Change of mental set requires the frontal lobe to inhibit the existent mental set and then activate a new mental set (198) (1083) (1365) (1951) and, again, this is subject to fatigue. Response inhibition has been quantified (563) (1025) (1027) (2569), as have response activation (757) and response error (1060). The frontal lobe orchestrates hypnosis through the distribution of activation and inhibition (240).

     The frontal lobe enables plans to be made (1037), through the activation of memories (199) (514) (1778), which feed forward what has happened in the past: this becomes feedback about what might happen in the future which may then influence motor responses (642).

     The frontal lobes enable consistency (1004).

     The frontal lobe can modulate responses to sensory stimuli. One example is when a frontal lobe reduces the likelihood of sensory stimulation by inhibitory priming of sensory nerves, a ubiquitous activity called presynaptic inhibition (969) (975) (1128). Another example is when an imperative sensory stimulus causes both outer frontal lobes to produce a momentary alerting response, which is seen in the electroencephalograph as a negative deflection, called the contingent negative variation (200) (1859). An example of an imperative sensory stimulus is a sudden loud noise.

     The frontal lobe includes visual (979) (907) (965) (994) (2224) (2742) (2809), and auditory and tactile (979) fields, within which other organisms can be perceived (201), and from which responses can be activated (1973) (2136). The amygdala characterises other organisms in degrees of safety (1513) (787) (1527) (2301), and transmits this information to the frontal lobe. Insofar as an organism experiences other organisms as safe, it will be able to experience itself within its visual fields to the degree that those organisms feedback perceptions about the organism itself (1464), rather than feed forward memories about themselves (448). Thus, the frontal lobe affords the opportunity for an organism to construct a map of itself within the outside world, albeit subject to the responses of other organisms (202) (203) (1608). As indicated in the quick guide, if a child is afraid then he or she will not construct a map of himself or herself in the outside world, or will merely pretend to do so, with dire consequences.

      An organism that is threatened keeps the parts of the brain associated with personal responses, that is the cingulate lobes, and with hostile instincts, that is the amygdalae, on hold until it produces its response, which could be fight, flight or continued retraction. Fight or flight would require the amygdalae to surmount any inhibition imposed by the inner frontal lobes through the uncinate fasciculi. Continued retraction, which might amount to a frozen state, would require the inner frontal lobes to maintain inhibition of the amygdalae through the uncinate fasciculi.

     The recognition of personal responses in others (1372) requires conversancy with one's own personal responses, which, in turn, requires a habitat in which those personal responses can be expressed, and identified as one's own (1653).

     The longer a child remains retracted from the outside world, then the less his or her cingulate lobes and amygdalae will be conditioned by the outside world, (1672) (855) (1670) and the less they will learn how to condition the outside world (1651) (311) (1038), perhaps due to reduced gaze fixation (1680) (1674) (1958). Given that the alerting inhibition by the outer frontal lobes of the rest of the brain evoked by an imperative sensory stimulus (1859) is produced initially by the outside world, the child will have less opportunity to learn that the inhibition is nonetheless the product of his or her own brain (204) (1711) (2151) (2421). There is a major difference between an adult human who finds the world a hostile place and an adult human who has learned that in certain hostile environments his or her brain will respond in a particular way, with inhibition of itself.

          A split in the brain: schizophrenia

     A child who perceives its outside world as unsafe may remain in a retracted, cryptic, state, so that, day-by-day, he or she will abide by the rules of the family (205), and will not display the personal responses of the cingulate lobes and the instinctive responses of the amygdalae (1728), but will keep these hidden, through inhibition by the inner frontal lobes (1568) (2462). The child will, in consequence, lack spontaneity. The potential for spontaneity will remain, however, because the child can choose to reveal his or her personal and instinctive responses at any moment. Bets are thus hedged, for which there are evolutionary antecedents (2196).

     In an attempt to fit in and feel less unsafe, the child may dissimulate: the child actively camouflages himself or herself (207) (700) through the production of the responses that reflect his or her perception of other people by his or her temporal and occipital lobes, which responses he or she thinks the other people in his or her unsafe outer world want to hear and see. The child may mimic siblings who appear favoured (206) (208), so that individuality is sacrificed for uniformity (1022). Then, to avoid any contradiction between these delayed responses and any possible immediate responses to the same auditory and visual stimuli, the child intensifies the inhibition of his or her own personal and instinctive responses. Effectively, the child reduces the signal to noise ratio, where the signal is the real child.

     A healthy sibling has been known to feign disturbance so as to confuse his parents, and thus keep them at bay, which dissimulation was confided convincingly to the psychiatrist (1209).

     Even more difficult for the child is incongruity between auditory and visual stimuli, which may produce a feeling of double bind, that whatever the child does at that moment is wrong. Initially, the child may respond to that part of the incongruity that induces fear (124), but catastrophic inhibition of that instinct may follow, in order to reduce conflict, ambiguity, and anxiety.

     Children in this mode can be heard describing themselves as how they think other people see them: "I am a bit naughty?" or: "I am a bit naughty!" or: "I am a bit .........naughty." There is a double meaning. The words are spoken on behalf of perceived other people, while the meanings conveyed by the punctuation marks are expressed by the embattled instincts of the child.

     The instinctually estranged child has a stark choice (489) (490) (501): face the fear of abandonment by getting into contact with your hostility through your amygdalae; or, in order to fit in, to feel less unsafe and to negotiate the pecking order, at least inhibit your amygdalae and thus your hostilty and come to lack spontaneity, and, at most, compound this lack of spontaneity with lack of authenticity, through the pretence that you are someone you are not. The child may compromise by keeping just within the prescribed boundaries but not without a degree of truculence, which is as healthy in the long-term as it is disruptive in the short-term (209). Paradoxically, then, the more biddable the child, the more disturbed the adolescent, because the more retracted the child, the less the personal and instinctive responses of the child will have been conditioned by the world (1672) (855) (1670), and the less the child will have learned how to condition the world (1651) (311) (1038), perhaps due to reduced gaze fixation (1680) (1674) (1958), and the more likely the child will have been to have acquired a hollow character (16).

     Some displays of truculence are clearly aposematic (571) (657), which makes diagnostic medical intervention all the more misplaced (588).

     The more dissimulated the child, the more mentally disorganised the disturbed adolescent (hebephrenic schizophrenia), while the less dissimulated the child, the less mentally disorganised the disturbed adolescent (paranoid schizophrenia).

     Before puberty, the habitat of the retracted, biddable child is relatively untroubled because of the efforts of the child to conceal any anger and thus to fit in. The child becomes conditioned to make personal responses less immediate, so that "I hate you, Daddy!" becomes "Mummy said she told you I cried." The child acquires a set of memories of having made personal responses less immediate. However, when the sex hormones of puberty bring instincts closer to the surface, what was easily put to the back of the mind at the age of seven intrudes at the age of seventeen. The part of the brain that has been inhibited so as to make dissimulation workable is unable to give any explanatory, personal content to the intensified feelings of arousal that are associated with provocative auditory and visual stimuli. The adolescent can only manage these feelings of arousal by making them less immediate, such as explaining them in terms of other people who are not actually present. "God, I hate my bloody Father!" becomes "I can hear my Mother talking to my Father about me."
     Whatever content of thought is chosen, it becomes an hallucination because the inhibition of personal responses as causes of that content gives that content the character of a perception, which is normally independent of personal antecedents (1850).
There is a lack of offsets, that is cancellation signals, that is corollary discharges, to distinguish personal thought contents from perceptions (41).
     The part of the brain that has survived through retraction starts to express itself in an unconditioned and thus idiosyncratic way (995), with delusions.

     Anatomically, the sex hormones of puberty stimulate the genitalia and, through these, the reticular network of nerves. The diffuse nature of the reticular network means that it is more difficult to inhibit than circumscribed structures like the cingulate lobes and the amygdalae (210). In addition, the sex hormones of puberty activate the brain directly, for example through each stria terminalis, so that arousal is brought closer to the inhibitory threshold set hitherto instinctively by the child, through the inner frontal lobes, to enable the child's perception of family life. This arousal enters the hippocampi through the brainstem and through the amygdalae (864), which are now more active than in years gone by because of hormonal stimulation by the proximate striae terminales. The points of entry of the arousal on the longitudinal axes of the hippocampi are determined by the auditory and visual stimuli in question. The arousal accesses the mesocortices through the mamillo-thalamic tracts (8) and accesses the neocortices through the sequence of CA1, subicular cortices, entorhinal cortices and perirhinal cortices (212) (527) (530) (211) (531) (532).
     To the degree that the perceived, personal arousal is not associated with perceived, personal, mesocortical input through the cingulum bundles, and a consequent response such as: "God, I hate my bloody Father!", because the cingulate lobes remain inhibited (213) (214), the hippocampi elicit remembered, impersonal, neocortical responses associated with the same degree of arousal (215), such as: "I can hear my Mother talking to my Father about me." The resultant hallucinations are not perceptions without external stimuli (211) (476), they are apperceptions without internal stimuli.
     The preponderance of auditory hallucinations reflects the verbal nature of the inhibited responses. Less commonly, somatic hallucinations are produced by inhibited motor responses (44).
     The occurrence of third person rather than second person auditory hallucinations reflects a greater degree of inhibition of personal responses.
     To the degree that the perceived, personal arousal activates the cingulate lobes for the first time in years, the perceived, personal, mesocortical input to the hippocampi is diffuse on their longitudinal axes and is outside the controls that the frontal lobes can exercise through the presubiculum (244) and the parasubiculum (H, volume 1), so that outlandish associations are formed between the neocortex, the mesocortex and the brainstem, such as: "Father (neocortex), you are making me (mesocortex) into a homosexual (brainstem)!" Cortico-cortical activations occur. During childhood, the pyramidal cells of the infragranular layers of the mesocortical cingulate cortices have been quiescent, due to focused inhibition by the outer frontal lobes, mediated by the inner frontal lobes, for example through the superior fronto-occipital bundles and through the cingulum bundles. Any activation of the pyramidal cells of the infragranular layers of the cingulate cortices has been from the supragranular layers of the neocortices (216) (679), perhaps layer 1, through the supragranular layers of the cingulate cortices: "top-down" rather than "bottom-up". These have been the neuronal equivalents of the driver going where he or she thought the driving instructor wanted him or her to go. Memories may have been formed of activations of the mesocortex by the neocortex, and these will have been stored in the supragranular layers, perhaps layer 3. Now, during adolesent arousal, the diffuse reticular network activates all parts of the brain in the direction brainstem to mesocortex and to neocortex. The unfamiliar activation of the infragranular layers of the cingulate cortices from below is experienced as something strange going on, that is delusional mood, which the adolescent tries to explain in terms of immediate surroundings, with consequent delusional perceptions and paranoid delusions. Insofar as memories have been formed of activations of the mesocortex by the neocortex and stored in the supragranular layers, these are experienced passively by the mesocortex now activated innovatively in the opposite direction, for example, as delusions of thought insertion and delusions of thought withdrawal. Motor acts that have been performed by the infragranular pyramidal cells of the cingulate cortices in response to the neocortices are expressed now as passivity phenomena (44). Innovative amygdalar arousal may reach the cerebral cortex directly, that is without traversal of the thalami, and may then cause delusions, with short latency.
     The cingulate cortex has been shown to contain at least 13 different subregions in the rat, while the anterior cingulate cortex has been shown to comprise two unique parts in the human (2401), which divisions would enable simultaneous inhibition and activation (877), perhaps using an electronic chip (2724).
     Hallucinations and delusions produce memories, and these are drawn on in future psychotic episodes.
     Prevention could begin before birth (1868) (2435) or during infancy (995) (1661), and, thereafter, could include probes for social inhibition, and for ambivalent anger, the latter tested with a GO-NO GO format. The probes should be human, and not inanimate, so that money would be unlikely to elicit differences between groups (995). For children at risk, neuroimagery and quantitative electroencephalography (2496) could address responses to anger more precisely, for example, in the anterior thalamic nuclei (384), with a view to neurofeedback (1464).
     Evidently, progress will require the combination of neuroimages and electroencephalography, rather than either technique alone (962) (463) (480) (1859) (2160) (2197) (2216) (2279) (2369) (2534) (2552) (2599) (2627).

     Deprived of introspective cues, the disturbed adolescent has to negotiate the outside world through memories of external landmarks (217).

     A corollary of the foregoing is that loss of contact with instincts is a risk factor for disturbance. Abuse, be it emotional, sexual or physical, conditions children not to respond to their instincts. A frightened child is dependent on those adults around him or her to recognise, contain, represent, and reflect back in tranquillity, those personal responses and memories that have been retracted through fear.

     The unconditioned and idiosyncratic expression of the part of the brain that has survived includes the delusion that the momentary, inhibitory response of the outer frontal lobes to an imperative stimulus is really outside interference with personal thoughts; this happens because the hitherto retracted brain has not been able to learn the difference between the provocative stimulus and the personal response (218).

     Insofar as the temporal precision of neuronal spiking responses is increased by inhibition (219), and insofar as inhibition actually moves a neuronal peak forward by decreasing the firing rate after a while (220), it amounts to disturbance if that inhibition is in the name of someone else: the driving instructor.

     The surviving brain may resort to angry overstatement, which may amount to violence and which is an understandable attempt to put the record straight. Just as understandable is the attempt of this surviving, uninhibited part of the brain to disinhibit the damaged, inhibited part of the brain with alcohol and recreational drugs.

     The disinhibition of inhibited hostility in schizophrenia may reflect the use of clozapine, a drug that suppresses bone marrow (221), and thus white cell precursors (222), some of which produce hostile responses (223).

     Some adolescents who have started to experience delusions and hallucinations have an inkling that something has changed, but they locate this mistakenly in the outside world (paranoid schizophrenia). Others have no such inkling (hebephrenic schizophrenia).

      Insofar as there is something to fear in the outside world (D, chapter 22) (224), then the more sensitive the child, the greater the risk of disturbance, because this child will be more likely to inhibit himself or herself than the less sensitive child, who does not detect the threat.

      If the child is more sensitive, then the greater the probability that there is something to fear in the outside world, and so the greater the risk of disturbance. Greater personal sensitivity is one of the ways in which a child may be distinctive relative to other members of a habitat or territory, including parents and teachers, whose envious responses make the outside world unsafe. The child thus chooses to remain in a retracted state: the driver is afraid of the driving instructor.

     The child may perceive its outside world as unsafe, not because of abuse or of envy, but because of lack of recognition. For example, a child who does not recognise itself at all in the outside world remains in its own autistic world (1671) (769) (1635) (1636) (2082), with inhibition of the personal responses of the cingulate lobes (1068), and of the instinctive responses of the amygdalae (1069) (1191). A child recognises itself in response to parental sensibility, which means that the parent inhibits his or her own responses so as to minimise apperceptions, and thus accommodate perceptions of the child (2829) (2845) (2862). Attempts to understand the evolution of autism in terms of formal intelligence have been inconclusive (1905), but not so in terms of intimation (2581) (2582) (2583) (2584). The parent's sensibility could be accessed through his or her perception of ∂x/∂t, where x is his or her child's vocal frequency or vocal intensity and t is time (2499), and through the Profile of Nonverbal Sensivitivity (S, page 308), The Autism Spectrum Quotient (2917), the Autism Quotient questionnaire (2922), and online communication technology (2918). How much of the parents' language is adjusted to the ages of their children when it is analysed by frequency and intensity (2579) (2608) (2580, page 1829) (2654) (2670) (2838)? Robots could be used as systematic comparisons with parents (2242) (2260), as could animals (2899) (2916). A child who has some recognition of itself in the outside world, perhaps through one of its parents, but who has become afraid of everyone else, relates naturally to the resonant parent but retracts and dissimulates with everyone else. The single, resonant relationship protects the child from hallucinations, and may have the same effect on delusions, although this requires openness. If the single, resonant relationship is covert, then delusions may actually be encouraged.
     The first appearance of hallucinations and delusions in adolescence may reflect the impact of the sex hormones of puberty on the differential expression of the genetic material inherited from each parent (281) (282) (283) (723), which would make particular sense if the prior chromosomal configuration had been inhibition of chromosomal material by the mother in terms of her own resources (680). This raises dark questions about the capacity of the mother to orchestrate chromosomes (725) so that the family has a sterile helper with increased vigilance (681) (698), effectively, an adaptive personality variation. Sex ratio variations (1273) (1274) (2272) (1367) (2109) (2391) that may be adaptive (2274) could be accessible through the introspection of energy intake (2473), of change in glucose levels (2262), and of hormonal fluctuations (1217) (1997) (2706), for example as a choice between: "I feel bad, so I need to create a male to protect me when I feel like this in later life..." (2161), associated with raised testosterone levels, and: "I feel good, so I need to create a female to assist with the rearing of more children...", associated with normal testosterone levels. Maternal effects have been studied in humans (2473) and in macaques (663), observed in reindeer (2149), modelled in vertebrates (2273) (2229), and inferred in birds (1644a) (1644b) (1644c) (1645) (1646). Paternal effects have been observed in birds (2681). Sibling effects have been studied in humans (2703). Siblings may be distinguishable by the degree of placental invasiveness, and thus by the degree of foetal antigen exposure, and consequent degree of downregulation of natural immune responses (1362).
     Schizophrenia is an extreme expression of discrepancy between the genotype and the phenotype. Flocks, herds, subcultures, groups, and families may collaborate to prevent the natural selection of an individual (226) (1361) (250). Christmas is reparative, and epideictic (D) (586). Sexual conflict reduces offspring fitness (1271). The advent of a child alters the social environment in which the phenotype of each parent's sex evolves (227). Conflicts between parents that embroil a child are risk factors for schizophrenia, and these may have differential effects between, and within, families (1723). In humans, the third party in a sexual conflict may be another facet of the personality of the first party or of the second party. If models of family life (1218) (1219) and of parent-offspring conflict (226) (1211) (224) (1652) are to apply to humans, then they need to include the configuration of the offspring's brain as a parent by the parent, through inhibition of the natural instincts of the offspring. The child learns a conditional strategy (228), unaware that hormones are going to change conditions. For example, if feelings that run high between the parents are managed through attribution to the child, who is acquiescent, then the child may lose individual fitness through that phenotype. The direct fitness of the child is sacrificed for the indirect fitness of the family (1849) (2520). The concept of inclusive fitness in humans (9) (1364) (2828) looks simplistic when the fitness of the child is increased by containment and protection from human predators outside the family during childhood (1269), only to be decreased thereafter because of the inhibition necessary to make the containment workable (710). The unlikelihood that a child would increase its parents' future reproductive fitness altruistically raises the whole issue of the capacity of the performer of an altruistic act to deliberate thereon.
     The stark realities of the psychiatric consulting room have been restated as genetic anthropomorphisms, such as "Parental antagonism,..." (716), "...disagreement between the maternally and paternally derived genomes of mothers..." (718), "...intra-genomic conflict..." (475), "intralocus sexual conflict" (2841), "...spiteful cytoplasmic elements." (720), and "...more 'abstemious' expression of maternally derived alleles and more 'greedy' expression of paternally derived alleles." (875).
     From the perspective of the life-time production of offspring, patients with schizophrenia can be seen as the products of group selection (competition between families), kin selection broadly defined (the disfavour of relatives inclusive of offspring) and weak individual selection (308). The family is divided into the reproductives, who will not develop schizophrenia, and the sterile workers (2495), who will develop schizophrenia. The carrying capacity of the family has been exceeded (1212). One of a number of siblings may be singled out because of his or her perceived Marginal Political Product (1213) at a given moment, which has environmental determinants (1272). The parental wish for platonic partnership and for care in later life may result in the production of helpful helpers (1214). Worker policing may take the form of disapproval of relationships outside the family (1215) (1943). Similar techniques may be used to cultivate non-relatives (1216), to the detriment of their mental health (2114). There is a form of enslavement (783). The delay in the onset of symptoms and signs until puberty argues strongly for genes that induce cooperation and reduce individuality, as distinct from genes that cause hallucinations.

     The concept of a learned Evolutionarily Stable Strategy (ESS), (205) (I, chapter 1) (229) looks unrealistic from the perspective of plasticity (732) without a currently obverse, inhibited, Evolutionarily Unstable Strategy (EUS). For every equilibrium between individuals, there will be, perforce, an equilibrium within each individual (230). Genetic and mathematical theories need a physical basis for how they work in the brain (1222) (1911), which, for an EUS, is likely to include synaptic inhibition through gamma-aminobutyric acid, and mirror neurones (31) (32) (33) (263).
     Differences between the neurones of patients and of controls may be correlates, or consequences, rather than causes. How long is needed before invasive family life produces developmental noise (333, page 295), phenotypic noise (333, page 295), phenotypic modifications (2341, page 583), cellular changes (728) (707) (390) (388) (737) (736) (379) (691) (963) (1821) (1852), chromosomal abnormalities (1036), or genetic alterations (324) (325) (708) (724) (938) (389) (378) (752) (940) (1885) (2277)? To what degree can the human habitat be an environment that engenders mutations, or alterations in gene expression (2476)? How many studies explore the impact of family life on the configuration and activity of alleles? If attempted disproof is the best way to reduce uncertainty (2167), then the failure to attempt disproof is consistent with a wish not to reduce uncertainty. Putative sensory encoding deficits in people with schizophrenia (902) may reflect the family who raised them. How is inherited genetic potential modified by activations and inhibitions, in particular those produced by ontogenetic selection pressures (307)? Genomic imprinting (283) (717) (680) (2084) may apply to children and to adults, perhaps through epigenetic mechanisms (385), conditioned by other members of the habitat. The identification of causative alleles is unlikely until family life is a controlled experimental variable (1929) (1930). RNA has been shown to induce retraction of synapses and of dendritic spines (1193), so that the stress of ontogenetic selection pressures could produce neuronal changes without involvement of nuclear DNA.
     The collaborative activity of groups may begin because those who harbour particular beliefs associate with one another; mutual reinforcement may lead to the beliefs becoming delusions, with loss of perspective about the idiosyncratic nature of the beliefs. Family life and terrorism may be viewed from this perspective.

     Schizophrenia is an extreme expression of the capacity to inhibit completely personal responses and memories, and thus the self, and to see a stimulus as accurately as possible, less extreme forms of which capacity confer an advantage, while, at the same time, leaving some of the self to experience that advantage (585) (2259) (2277). The greater the capacity to inhibit oneself, then the greater the dependency on others to represent the self during formative years. Once schizophrenia is established, then the probability of auditory hallucinations is a function of the sum of personal contacts that inhibit spontaneity minus personal contacts that enable spontaneity. Critical comments by important family members are a subset of this function (231).
     The schizotypy described in reference (585) has been shown to include larger volumes of the bilateral middle frontal gyrus, than controls (859). Negative frequency-dependent selection may operate (948).
     Atypical antipsychotic drugs have parasympathetic effects such as salivation, rhinitis, increased appetite and urinary incontinence, which may be the autonomic expression of spontaneity, the drugs having disinhibited the cingulate lobes (20). The circuitry may include the bone marrow (270). Vagus nerve stimulation should have something to offer (271) (290), because of the activation of inhibited personal responses (272) (293) (454).
     The claim that the anti-psychotic drug, haloperidol, inhibited replication of the parasite Toxoplasma gondii (796) was based purely on behavioural inference, with no accessible evidence of a direct effect of haloperidol on the parasite, so that there were no significant implications for the aetiology and treatment of schizophrenia.
     Attempts to represent schizophrenia as primarily a cognitive disorder (1425) (2331), are likely to be unconvincing. Schizophrenia is not a neurodegenerative disorder like Alzheimer's disease (2041).

     The evolution of the brain may have contributed to what is now called schizophrenia (1934). The sulci, the gyri and the insular operculae attest to the rapidity of expansion of the neocortex, as does the consequent obliteration of the dorsal hippocampi and the resultant loss of new neurones that they could have provided (273) (330): the main input pathway to what remains of each hippocampus has to perforate the main output pathway to reach its target (274) (1641). All of this stretches evolutionary teleology to the limit. The detailed map of the world that the neocortex affords (575) is futile if one cannot find oneself in it. The implication is that we may be at a point in time when evolution of the brain has got ahead of itself (1691) (2291), which we need to offset with the clearest possible establishment of personal responses and instincts before parental attempts at contemporary characterisation. Targets and standardised measures are means to the end of the relationship between a pupil and a teacher, and are not ends in themselves. The dangers of expansion of the neocortex, at the expense of the mesocortex and of the allocortex, increase as organisms become more altricial, and less precocial.

           Vulnerability to loss: mood disorders.

    The inner side of each cerebral hemisphere mediates personal responses (232) (1079) (687) (1017) (2522), including those from the cingulate lobe (CL) (922) (528) (234) (235) (529) (19) (559) (2147) (2595) (2688) (2903) (2913), which can be both activated and inhibited by the front end of the inner side of each cerebral hemisphere, the inner frontal lobe (IFL) (237) (236) (238) (865).

Figure six

[Back to Figure four]

     The inner frontal lobe and the cingulate lobe can be both activated and inhibited in response to the auditory and visual stimuli of the outside world by the outer frontal lobe (OFL) (1038) (1365) (1648). Thus the inner frontal lobe has an intermediary relationship between the personal responses of the cingulate lobe and the outside world (1047) (1225) (870) (1392) (996) (1801) (2423) (2647), which is mediated by the outer frontal lobe (21) (1662) (1793) (1861) (1865). For example, the inner frontal lobe restrains the spontaneity of the cingulate lobe (1051) until the outer frontal lobe signals that the outside world is safe (2108), whereupon the cingulate lobe can express itself through play and creativity (1007) (1393) (1819) (2017). The right inner frontal lobe has been implicated in stress responses (1338) (1731), and in social responses (1567). The right outer frontal lobe has been associated with insight (1701). The left outer frontal lobe has been associated with truth (1754).

     The cingulate lobe, at least in its motor area, distinguishes clearly between the Ready and the Steady and the Go of Ready Steady Go (1059), but distinguishes less clearly between different spatial locations of Ready Steady Go (899), for which it requires, presumably, the intermediary activity of its inner frontal lobe.

     It is normal to do different things with the two cerebral hemispheres of the brain, at the same moment, in safety (266) (529), and in vigilance (1586). In immediate danger, the two cerebral hemispheres of the brain probably act as one, so that, at the same moment, both inner frontal lobes and both cingulate lobes are inhibited by the alerting response of both outer frontal lobes.

     During formative years, the inner and outer frontal lobes are activated and inhibited by real people, but if the child is to become self-sufficient, then he or she has to learn to activate and inhibit his or her own frontal lobes, and to manage conflict (1698), independent of other people (749). This will equip the individual with response inhibition, focus, working memory, motor response potential, mental set, planning, consistency, and mapping.

     It is likely that the degree of unowned inhibitory capacity sets a phenotypic limit on the genotype.

     The capacity to vary one's responses when the environment changes, within one's habitat and within one's territory, in the absence of other people, is called homeostasis.
     It is likely that the costs of variation are set against the benefits. Humans expend energy to maintain a relatively constant body temperature in response to environmental changes, which enables them to function within a range of environmental temperatures. Some animals do not expend the energy necessary to function in cold environments, and hibernate. The more motor responses that a change of environment requires, then the more predation risks and the more physical costs (2487), seen in humans as the relatively stressful move of house and change of job. Better to adapt inside one's head than to move physically.

     The more that an individual remains dependent on other people to activate and inhibit his or her frontal lobes, then the more he or she will be vulnerable to the absence or loss of those other people, with consequent depression.

     Homeostasis is impeded by embroilment of children with parents (226) (2426), and such embroilment runs in families, as do the depression and mania associated with impeded homeostasis (239). Examples of embroilment include the adult who has consigned painful childhood memories to the back of the mind, only to find that parenthood brings the memories to the front of the mind, with exposure of his or her child to his or her own painful childhood memories, and so on. Again, reversal of the roles between the inner frontal lobes and the cingulate lobes during childhood may bring some depression to parenthood because of the realisation of the loss of spontaneity occasioned by protective responses during childhood, which pattern may then be repeated, and so on.

     Sometimes, an individual who has become homeostatically challenged due to loss, may make a determined attempt to carry on as if nothing has happened. This response pattern is extremely common, and can, at times, be productive (347) (1584). However, the more that an unmet visceral need is due to lack of a dependent relationship, then the more difficult is the corrective action, the more frantic and unpredictable are the attempts at correction and the greater is the risk of mania (241). Overactivity of children has the same import as mania in adults; the avoidance of emptiness. As for adults, there may be absence of someone who is necessary to complete a circuit that will meet an unmet need. Amphetamines are effective because they activate nerves that contain dopamine.

     The appearance of mania is of too much nervous energy in too few circuits, and the appearance of the lachrymose, therapeutic moment when loss is faced is of circuits closed hitherto, opened anew, so that the current level of nervous energy falls through increased containment.
     The verbal emphasis of pressure of talk and flight of ideas conveys that the language circuits of the cerebral cortex are open. The wish to gloss over loss and unmet need conveys that the visceral circuits driven by the basal ganglia are closed. Working memory may be overused to avoid introspection, with consequent distractibility (287).
     The hippocampi are possible sites for the machinations of mania. Visceral input circuits from the brainstem and from the olfactory cortex could be inhibited by the amygdalae (242), or by the cerebral cortex (244), so that incoming stimuli would be restricted to auditory and visual. The site of inhibition could be where the Schaffer collaterals synapse with the pyramidal cells of CA1 (275) (276), but there are other possibilities with respect to topography (1468e), laminae (278) (243) and nerve endings (279).
     Attempts to relate decisions about war to overconfidence need to address the essentially manic failure to consider someone else's losses as if they are one's own. The statement that mentally healthy people tend to exibit "positive illusions" is questionable, hence the use of quotation marks (1576), which shows a lack of confidence.

     Homeostatically adjusted adults may elect to participate in a division of labour (245) (1451) (341) (1624) (577) (804), when they choose to depend on someone else for some of their responses. Loss of that someone else, through bereavement, is usually followed by depression for about six months, the length of time it takes to regain mastery of the parts of the brain that hitherto required activation by the deceased. Depression can also occur sporadically in an adjusted person because of a wish to protect a loved one, often a child, from anger (17). The necessary inhibition of the amygdalae spreads to the hypothalami, where it affects body chemistry and thus functions such as sleep, appetite, and hormone release, and also cellular defences, so that damaged cells are not removed, with predisposition to cancer (862). Again, guilt about one's responses may lead to depression because of inhibition of the brain by the brain, specifically of the cingulate lobes and amygdalae which delivered those questionable responses, by the outer frontal lobes, which represent the people to whom the responses were delivered. The different antecedents to depression may help to explain the inconsistent and contradictory structural findings (239) (641) (327) (7) (328) (2589).

     A division of labour is achieved at a cost to the participants (2502). For example, in adult humans, the male partner may be dominant and the female partner may be submissive, which, in principle, requires the male to do the work of maintaining preparatory, dominant responses and of inhibiting submissive responses, and requires the female to do the work of maintaining preparatory, submissive responses and of inhibiting dominant responses. Compare regression, in which one partner tries to get the other partner to do as much of the work as possible.

     The distribution of responses in a division of labour necessitates genetic inhibition, that is the inhibiton of genes that produce the responses to be delivered by the other party, and genetic activation, that is the activation of genes that produce the responses to be delivered by oneself. Each inhibition and activation is likely to have chemical and hormonal consequences for both genders (2392), with obligate chemical time constants necessary for the inhibitions and activations to be constructed at a molecular level.

     Spite in animals is unlikely to be accessible without clarification of whether spite entails harm to the self, as well as to others (822) (982); cost to the self, as well as to others (311); or a lack of benefit to the self, as well as to others (719). For a review, see reference (1039). Displacement activities require consideration (321). Calculation of the cost needs to include the work of inhibiton of hostility, relative to its expression, with particular reference to subsequent predation risk, in terms of disclosure and lack of readiness. For humans, the timing of the expression of an emotion is significant (854), with particular reference to the cost of containment of a bad feeling relative to its expression, and this needs to be included in analyses of punishment (80) (2130) (2330) (2357) (2595) (2704) (2755) (2843). Complete lack of expression carries the risk of depression. Suicidal gestures may harm others more than the self, and may even benefit the self, from the perspective of the costs of working memory and of the division of labour. Some forms of jealousy are rational, in that there are continued costs, but loss of benefits.

     It is unlikely that "treatment-resistant depression" and the anomalous steroid hormone response in depression will be clarified until anger is included as a controlled variable in the experimental design.
     Evidently, depression, often consequent upon loss, may affect both those who have attained autonomy in the past, and those who have not attained autonomy in the past, and as such, the occurrence of depression does not distinguish between these backgrounds.. The occurrence of mania does, however, suggest such a distinction, because it discloses the preference to gloss over loss, even when invited to reflect on this in tranquillity, which invitation is usually accepted by the bereft stoic. The difference between so-called bipolar depression and unipolar depression may, to a degree, reflect the difference between depression without prior homeostatic adjustment and depression with prior homeostatic adjustment, respectively. This is a cause for concern, because if a history of mania increases the likelihood that someone with depression receives lithium, then the very person who needs counsel, and who is done a disservice in the long run by the use of explanatory medication, is setting off in exactly the wrong direction. The journey may be hazardous. Of all the chemicals introduced into medicine through poor science, lithium is one of the most dangerous. The overview in reference (10) still applies: population studies still do not show convincing evidence of the effects of lithium over time (246); the reference to a trial as "double-blind" when lithium had been found in the serum of four of the patients who had been given placebo indicated a nadir of wishful thinking that beggared belief, but this preference for fantasy endures (11). On an individual basis, lithium may be helpful because it obliges homeostatically challenged patients to follow a routine, but there are safer ways to achieve autonomy, such as religion tempered with humility, and cognitive therapy (937).

     The diagnostic category called "manic-depression" is simplistic because it fails to ascertain the degree to which the patient's mental health has evolved prior to diagnosis and thus it fails to address the management and the prognosis: has the patient been homeostatically adjusted in the past, because if so, then this can be relearned, whereas if not, then it will have to be learned for the first time, with family involvement.

     Not to be confused with depression is regression, which occurs when adult humans choose to relinquish some of their customary self-control and to invite other humans to take over. This voluntary, adult form of regression is not to be confused with the involuntary, developmental regression of a child (1682). Adult, voluntary regression is transitory, and immediate features include fleeting eye contact, faintness of voice (2741), flexed posture and failure to produce complete sentences. The first person singular personal pronoun may be particularly inaudible and verbs may be in the passive voice. Anxieties shoot up and are moved on rapidly to someone else. Disagreeable experiences are off-loaded verbally so that they can be heard coming in through the ears, and, as such, disowned by the regressor as outside him or her. Regression often has a sexual element, which may have a basis in cooperative breeding (J, chapter 8) and in anisogamy (J, chapter 5). Regressive relationships evoke producers and scroungers (249), and exploitation (R, page 172) (J, chapter 6).
     Regression can be seen in the market place. An indecisive operative can reach a decision quickly if he or she is able to induce responses in a colleague.

Figure seven

As shown in figure seven, the shift of either the + or the - of the + or - conflict from the part of the brain associated with personal responses to the part of the brain associated with the outside world frees the part of the brain associated with personal responses to be decisive in the opposite direction.
An unfocused operative can concentrate by causing disruption in those nearby.

Figure eight

As shown in figure eight, the limited inhibitory capacity of the inner frontal lobes is unable to provide the necessary focus. The disruption activates further inhibitory capacity in the outer frontal lobes, which augments the existent but insufficient inhibitory activity of the inner frontal lobes, and enables concentration; effectively, the outer frontal lobes dampen internal noise. This phenomenon is recognised in science (1419), and has been called stochastic resonance (251) (1229) (2929). Noise may improve the sensitivity of circuitry that has adapted to stimuli (2317).
     Regression can be collective (280), which is an example of the lack of capacity to vary or not one's responses in changing circumstances within one's habitat and within one's territory in the presence of other people, and which is likely to be a predictor of the mood disorder of anxiety.
     Regression may have genetic correlates (646).
     The habitual use of other people for the purpose of definition of oneself is, like the occult, a function of limited introspective identity, and invites the uncomfortable aphorism: "I am who I am with." Transitory occupations and relationships may give an illusory experience of oneself through perceptions of other people's loss of one. A network model of human relationships would emphasise the degree of interaction with other people that is necessary before one can communicate with oneself, inclusive of one's visceral self: the realisation of any of tense muscles, tight sphincters, palpitations, bated breath, dry eyes, dry mouth, abdominal sensations and genital engorgement.
     The numinous tendencies of humans are essentially regressive, and account for phenomena such as the Barnum effect (2557) (R, page 171), for recourse in magical solutions to stress (2430) (R, page 174), and for reduced support for some forms of punishment (2827).
     "Give me a reminder..." is a regressed attempt to increase one's working memory capacity through someone else. "Make sure I am up in the morning..." is a regressed attempt to improve quality of sleep, as is the articulation of stresses to someone else, just before one retires to bed.
     Electronic mails and mobile telephones facilitate regression.
These are examples of the lack of capacity to vary or not one's responses in changing circumstances within one's habitat and within one's territory in the absence of other people; this is a risk factor for mood disorders, and it varies with age and with gender.

     Dependency on another organism may be the result of a decision to take part in a division of labour (2558), or it may be the result of a decision to regress, or it may occur spontaneously. Irrespective of their antecedents, such episodes of dependency can be remembered (1210), and can thus be expected in the future, so that cooperation is hardly surprising, and does not require the invocation of anthropomorphic genes (252) (1224) (2366) that are unlikely to explain very much of the variance in the real world, or of artificial games (1000) (1578) (1984) (2366) (2785) (2834), the results of at least one of which have been related to pictures of sexy women or lingerie, and to digit ratio (1282). Spontaneous dependency may be construed as inversely related to differentiation, inclusive of sex chromosome differentiation.

     Memory of dependency is central to the production of supposedly altruistic acts (78) (79) (576) (2712), which are also motivated by territory protection (95) (816) (75) (253) (1760) (1814) (1884), and by the cultivation of reputation (304) (1223), of good standing (305), of status (498), of reproductive promise (812) (840) (2276) (2623), and of image (1573) (306) (1008), which latter may be exploited subsequently (383) (1817) (2261). Brain images have identified circuitry consistent with memories (254). Spontaneity, as distinct from memory, is also important in altruistic behaviours (80), one motive for which is the enlivenment of one part of the actor's brain by another part of the actor's brain through the elicited responses of bystanders. It is likely that humans vary in their spontaneous altruistic behaviour over time.

     To date, theories about the stability, over time, of selection, cooperation, and altruism, have been based on presumptions about the stability, over time, of individuals. This has resulted in attempts to reconcile the reality of internal conflict with evolutionary principles (557). The definition of mental health in this text includes a social component that entails reference to other people, which is consigned during development (2580) and is then elective during adult life. Stability over time is thus a function of other people, such that we are who we are with. True, as adults there are nodal points at which we choose with whom to be, but between those points, our fitness depends on the behaviour of others (711) (2440), to the degree that activation of one part of one's brain by another part of one's brain can be conditional upon the intermediary activity of someone else (M) (2005). This is why potential partners appraise each other prior to commitment (653), to ensure that the other party will activate the part of the brain that has to be inhibited if procreation is to occur.
     Dependency on others brings fluctuations in one's adjustment, and thus unfitness, as a function of the variations within and between those others, exemplified by changes in females due to lunar hormonal variations. We need other humans to provide foci for the expression of our personal and visceral responses, which, otherwise, reverberate intrusively, and produce symptoms such as muscular tension, headache, and nausea. Some occupational roles may evolve to produce an array of inhibitions and dissimulations that are unworkable, for example, because of contradictory responses with family life, so that one's role in the territory is in conflict with one's role in the habitat. Crossword puzzles on the way home from work convey a hard, inhibited, day at the office, and may not be the best preparation for one's return home.

     Natural selection in humans is not based on the survival of the fittest, it is based on the survival of the less unfit. One's unfitness may be increased or decreased by kin, friends and acquaintances alike (2002). Fitness is likely to depend on the ability to distinguish between other individuals' kin, friends and acquaintances (2141), which, in turn, is likely to depend on memory, and thus on brain size (2142). Supposedly altruistic acts delivered to strangers who one will not meet again are a function of the present mental state, especially the part of one's brain that is activated by the stranger at the moment of altruism (M). Supposedly altruistic acts delivered to people who one will meet again are calculated, to reduce personal unfitness. The capacity to perceive personal unfitness is increased by the capacity to see and hear oneself through the eyes and ears of other people within one's habitat and within one's territory, and thus by mental health. If "...the fitness a* of an individual is treated as the sum of his basic unit, the effect ∂a of his personal genotype and the total eº of effects on him due to his neighbours which will depend on their genotypes: a* = 1 + ∂a + eº." (9), then ∂a can have a negative value > –1 such that 1 + ∂a is negative, and is a measure of unfitness, such that eº is needed for immediate survival, and thus for enduring fitness. Success is the ability to learn from failure.

     Sexual selection in humans includes the choice of a partner who facilitates one's mental health.

     Unlike his contemporary Charles Dickens (1536), Charles Darwin did not include mental illness in his scheme of things. Nor, one suspects, did Darwin's epigoni.

           ADULT ADJUSTMENT.

     Successful human development requires that the personal responses and instincts of a child are expressed to the degree that they can be demonstrated to the child as his or hers: this is the capacity to see and hear oneself through the eyes and ears of other people. Parents and teachers are then able to provide the child with a model of how to condition his or her own personal responses and instincts using his or her own frontal lobes: this leads to the capacities to vary or not one's responses because of what one sees and hears through the eyes and ears of other people, and also to the capacities to orchestrate one's responses in changing circumstances in the absence, and in the presence, of other people. As development proceeds, parents and teachers model increasingly the variability of the outside world (428), to reduce behavioural carryover across contexts (342).

     Adult adjustment requires the frontal lobes to mediate between personal responses and instincts on the one hand and social imperatives and inhibitions on the other hand.

     The adjusted human allows time to reflect, integrate, wind down and rehearse in repose every four to six hours (255) (1751), to visualise who, and where, he or she has been (750), with reference to other people and to achievements, during that period. This protects the adjusted human from memories fed forward by other people (2230), and from regressive exploitation (1689). At the same time, this adjusted human identifies, and then makes decisions about, personal and instinctive responses to sensory stimuli, inclusive of proactive resolution of conceptual conflicts and then of imaginal task implementation (984) (1314) (2869). This adjusted human knows that personal and instinctive responses represent unfulfilled potential (256), whether they are expressed in a particular setting or not, and that if they are not recalled in tranquillity and then channelled into the frontal lobes of the cerebral hemispheres then they will be lost to conscious control (257) (2873). The "Deliberation-without-attention" effect demonstrated in shopping (553) should be assumed not to apply to relationships, at least until after deliberation with attention to what is me and what is not me.
     A written variant of reflective integrity has been demonstrated (414).

     Examples of reflective activity are prayer, meditation, relaxation and self-hypnosis (258) (2213).

     If the capacity to reflect and focus is developed while still young, it may pay dividends later in life (452), and it may prolong life, if one's body is conditioned to different emotional responses, so that, for example, one's body can distinguish between the nervous reaction to acute anger and the nervous reaction to acute haemorrhage (661) (778). Some of the beneficial effects of regular exercise may be due to a nerve growth factor (851) (852), and to tolerance to change (1811). Pain is reduced if anxiety is managed (1704).

     Sleep affords assimilation of personal and instinctive responses, but without the awareness afforded by reflection in repose. Alcohol removes inhibitions chemically, ergo in vino veritas, although how much of the veritas is recalled in tranquillity, and is therefore owned, is another matter. Other chemicals affect personal responses and instincts, especially on Midsummer Nights.

     Corporate activity may be sought to manage inhibited personal responses and instincts, hence the occurrence of religions, cults, nepotism, and terrorism. A group may believe that a particular object is talismanic in the removal of inhibitions, and this may reach delusional intensity with respect to the rest of Society.

     Relationships between organisms may be adaptive in the mediation between personal and instinctive responses on the one hand and imperatives and inhibitions on the other hand (2099), conditional upon the use of time (259) and the demands of place, such as whether one lives on a prairie or in a meadow (302). One human may condition another human to orchestrate his or her personal responses and instincts, and this division of labour may begin with the experience of "love" (640) (261) (2667), one meaning of which is a simultaneous realisation by two humans: "I know that you know that I am inhibiting my personal responses and instincts so that your personal responses and instincts can be expressed, and I know that you know that I know that you are inhibiting your personal responses and instincts so that my personal responses and instincts can be expressed." This is mutual genetic inhibition, and mutual containment of consequent paranoid misperceptions. Sufferers from hallucinations find this reciprocity difficult, because the inhibition required increases the probability of hallucinations, so that a more egoistic style prevails (318) (260) (1226).

     The conditionality of the human courtship is the homologue of the preparatory, exploratory activity of birds (653), and probably bees, and educated fleas, amongst others: "If I put part of my brain into abeyance in order to have children, will you look after it?"

     Stress promotes love (262). When the environment changes abruptly, prior oscillatory activity becomes maladaptive and hazardous. Sex is a circuit-breaker (2453) (550).

           A QUICK GUIDE TO THE PREVENTION OF MENTAL ILLNESS.

     Parents may wish to consider the following questions.

     Is my child learning the potential difference between the "I" in "I see you." and the "me" in "I see you seeing me."?

     Is my child clumsy or accident-prone, perhaps because of haste that exceeds the capacity of the brain to streamline motor responses? If so, should I address this through more play activities in safe areas?

     Does my child recognise that someone else can experience the same circumstances differently at the same time? Does my child recognise that he or she can experience the same circumstances differently at different times? If not, do I need to look at the consistency in my child's world?

     Does my adolescent child recognise that changes of mood can cause him or her to experience the same circumstances in different ways at different times? If not, should I try to illustrate this through personal example?

     How much do the people in my child's world feed back perceptions of my child to my child, and how much do they feed forward personal memories onto my child, who they misperceive in consequence? Should I decide to make an immediate detraction if I hear myself or anyone else construe my child in terms of personal memories? (..."you remind me of my mother"... ).

     Is my child able to express his or her personal responses and instincts to the degree that they can be conditioned? If not, is my child too good to be true and too good for his or her own good? Is my child afraid to say how he or she really feels, perhaps for fear of upsetting me? Does my child tell me what he or she thinks I want to hear, and can I hear double messages that intimate the real feeling? If so, should I articulate what else my child might be feeling at such a moment?

    Is my child's apparent misbehaviour really a cry for recognition? If so, should I review the formats available to my child on the basis that they do not enable my child to be himself or herself?

    Does my child prefer to let other people do for him or her what he or she can do perfectly well for himself or herself? If so, does my child need more peer group activities?

    Does my adolescent child have the capacity for closure, which is the completion of what he or she has started? If not, should I consider an orchestrated, family approach?

    Does my adolescent child gloss over difficulties that are obviously upsetting, to the degree that he or she becomes driven and accident-prone? If so, should I encourage my child to articulate the difficulties at a quiet moment?

    Does my adolescent child understand the benefits of reflection every four to six hours? Specifically, does he or she understand the need to visualise where he or she has been in the last four to six hours, and then to consider who he or she has been, with reference both to other people and to his or her achievements, during that period? Does he or she understand the need to make decisions about personal responses and instincts during that period and then implement those? Does this adolescent child realise that he or she can orchestrate the cells of his or her brain to meet new demands within minutes?

Figure nine

          EVOLUTIONARY THEORIES AND MENTAL ILLNESS.

     The teleology of survival of the fittest puts the individual into conflict with the family. A theory of survival of the less unfit, who has become less unfit through his or her family, does not put the individual into conflict with the family, but enables cooperation and altruism within the family, and thus increases the likelihood of enduring reproductive fitness in the distant future.

     The theory of inclusive fitness in humans means that the family improves its fitness at the expense of one of its members, who may be a child, and who may not have any choice (2828).

     The theory of exclusive fitness is that the families of patients with mental illness behave in ways that reduce the patients' reproductive fitness. The frequency of mental illness remains constant within the population because the major causes of mental illness are developmental, not genetic.

     The ideal that our genes live on after we die is an intellectually defended version of Life After Death. Genetic similarity brings physical similarity, which may make our mental lives worse, not better, because it invites our family to imagine that we are more like them than is, in fact, the case, with consequent embroilment and lack of autonomy.

     Explanations of animal behaviour in terms of future reproductive fitness risk the intellectual anthropomorphism that animals plan their futures (2157, page 22). For example, ritual fights between members of the same species may amount to practice for real fights between members of the same species (18) (1559) (610) (685) (1107) (2204) (2344), and for real fights between members of different species. Reproductive fitness in the future requires survival in the present. Reproductive fitness may be an epiphenomenon (2470).

     The notional direction of the relationship between evolution and behaviour may depend on one's professional training, for example as an evolutionary biologist or as a physiological and functional ecologist (2408, page 357).

          ETYMOLOGY

     The Greek or Latin origin of some of the unusual terms in this text is as follows:-

Adrenal - above the kidney.

Amygdala - almond.

Apperception - towards perception.

Caudate - having a tail.

Cerebellum - little brain.

Cerebrum - brain.

Cingulate - girdle.

Claustrum - enclosed place.

Cochlea - snail shell.

Corpus callosum - hard body.

Cortex - outer part.
     neocortex - new cortex.
     mesocortex - middle cortex.
     allocortex - other cortex.

Delusion - from a game.

Depression - pressed down.

Endocrine - sift within.

Exocrine - sift outside.

Frontal - of the forehead.

Ganglia - knots.

Glia - glue.

Globus pallidus - pale sphere.

Hallucination - wandering in the mind.

Hebephrenic - of youthful mind.

Hippocampus - sea-horse.

Homeostasis - like standing still.

Hormone - set in motion.

Hypothalamus - below the thalamus.

Insula - island.

Mania - madness.

Medulla oblongata - oblong inner part.

Migraine - half skull.

Occipital - of the back of the head.

Ovary - egg.

Pancreas - all flesh.

Paranoid - beyond the mind.

Parathyroid - beside the thyroid.

Parietal - of the wall.

Pheromone - transfer hormone.

Pineal - pine cone.

Pituitary - secreting phlegm.

Placenta - flat plate.

Pons - bridge.

Putamen - shell.

Regression - going back.

Reticular - net.

Schizophrenia - divided mind.

Stochastic - conjecturing.

Stria terminalis - terminal furrow.

Substantia innominata - nameless substance.

Substantia nigra - black substance.

Synapse - join together.

Temporal - of the temple.

Testis - witness, to virility.

Thalamus - inner chamber.

Thyroid - oblong shield.

Uncinate fasciculus - hooked bundle

Vermis - worm.

Michael Robinson © 2003.

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(467) Comparative gene expression analysis of blood and brain provides concurrent validation of SELENBPI up-regulation in schizophrenia.   Glatt SJ, Everall IP, Kremen WS, Corbeil J, Sasik R, Khanlou N, Han M, Liew CC and Tsuang MT.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 15533-15538.

(468) Brain activity associated with expectancy-enhanced placebo analgesia as measured by functional magnetic resonance imaging.   Kong J, Gollub RL, Rosman IS, Webb JM, Vangel MG, Kirsch I and Kaptchuk TJ.   2006.   Journal of Neuroscience, volume 26, pages 381-388.

(469) Tactile spatial attention enhances gamma-band activity in somatosensory cortex and reduces low-frequency activity in parieto-occipital areas.   Bauer M, Oostenveld R, Peeters M and Fries P.   2006.   Journal of Neuroscience, volume 26, pages 490-501.

(470) Listening in silence activates auditory areas: a functional magnetic resonance imaging study.   Voisin J, Bidet-Caulet A, Bertrand O and Fonlupt P.   2006.   Journal of Neuroscience, volume 26, pages 273-278. 

(471) The role of the amygdala and olfaction in unconditioned fear in developing rats.   Chen SW, Shemyakin A and Wiedenmayer CP.   2006.   Journal of Neuroscience, volume 26, pages 233-240.

(472) Under the curve: critical issues for elucidating D1 receeptor function in working memory.   Williams GV and Castner SA.   2006.   Neuroscience, volume 139, pages 263-276.

(473) Mental chronometry of target detection: human thalamus leads cortex.   Klostermann F, Wahl M, Marzinzik F, Schneider GH, Kupsch A and Curio G.   2006.   Brain, volume 129, pages 923-931.

(474) Spatial effects in social dilemmas.   Hauert C.   2006.   Journal of Theoretical Biology, volume 240, pages 627-636.

(475) Optimization of inclusive fitness.   Grafen A.   2006.   Journal of Theoretical Biology, volume 238, pages 541-563.   See "intra-genomic conflict".

(476) Neural activity in speech-sensitive auditory cortex during silence.   Hunter MD, Eickhoff SB, Miller TW, Farrow TF, Wilkinson ID and Woodruff PW.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 189-194.

(477) Banishing the homunculus: making working memory work.   Hazy TE, Frank MJ and O'Reilly RC.   2006.   Neuroscience, volume 139, pages 105-118.

(478) Investigating principles of human brain function underlying working memory: what insights from schizophrenia.   Honey GD and Fletcher PC.   2006.   Neuroscience, volume 139, pages 59-71.

(479) Working memory for visual objects: complementary roles of inferior temporal, medial temporal and prefrontal cortex.   Ranganath C.   2006.   Neuroscience, 139, pages 277-289.

(480) Trial-by-trial coupling of concurrent electroencephalogram and functional magnetic resonance imaging identifies the dynamics of performance monitoring.   Debener S, Ullsperger M, Siegel M, Fiehler K, von Cramon DY and Engel AK.   2005.   Journal of Neuroscience, volume 25, pages 11730-11737.

(481) Early and late mechanisms of surround suppression in striate cortex of macaque.   Webb BS, Dhruv NT, Solomon SG, Tailby C and Lennie P.   2005.   Journal of Neuroscience, volume 25, pages 11666-11675.

(482) Functional magnetic resonance imaging shows oxytocin activates brain regions associated with mother-pup bonding during suckling.   Febo M, Numan M and Ferris CF.   2005.   Journal of Neuroscience, volume 25, pages 11637-11644.

(483) CNS projections to the pterygopalatine parasympathetic preganglionic neurons in the rat: a retrograde transneuronal viral cell body labeling study.   Spencer SE, Sawyer WB, Wada H, Platt KB and Loewy AD.   1990.   Brain research, volume 534, pages 149-169.

(484) 2003 Wolff Award: possible parasympathetic contributions to peripheral and central sensitization during migraine.   Yarnitsky D, Goor-Aryeh I, Bajwa ZH, Ransil BI, Cutrer FM, Sottile A and Burstein R.   2003.   Headache, volume 43, pages 704-714.

(485) Patterns of fos expression in the rostral medulla and caudal pons evoked by noxious craniovascular stimulation and periaqueductal gray stimulation in the cat.   Knight YE, Classey JD, Lasalandra MP, Akerman S, Kowacs F, Hoskin KL and Goadsby PJ.   2005.   Brain Research, volume 1045, pages 1-11.

(486) Distribution of fos-like immunoreactivity in the medullary and upper cervical dorsal horn produced by stimulation of dural blood vessels in the rat.   Strassman AM, Mineta Y and Vos BP.   1994.   Journal of Neuroscience, volume 14, pages 3725-3735.

(487) Unitary hypothesis for multiple triggers of the pain and strain of migraine.   Burstein R and Jakubowski M.   2005.   Journal of Comparative Neurology, volume 493, pages 9-14.

(488) Substantia innominata: a notion which impedes clinical-anatomical correlations in neuropsychiatric disorders.   Heimer L, Harlan RE, Alheid GF, Garcia MM and de Olmos J.   1997.   Neuroscience, volume 76, pages 957-1006.

(489) Central circuits mediating patterned autonomic activity during active vs. passive emotional coping.   Bandler R, Keay KA, Floyd N and Price J.   2000.   Brain Research Bulletin, volume 53, pages 95-104.

(490) Parallel circuits mediating distinct emotional coping reactions to different types of stress.   Keay KA and Bandler R.   2001.   Neuroscience and Biobehavioral Reviews, volume 25, pages 669-678.

(491) Direct neurophysiological evidence for spatial suppression surrounding the focus of attention in vision.   Hopf JM, Boehler CN, Luck SJ, Tsotsos JK, Heinze HJ and Schoenfeld MA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 1053-1058.

(492) Emotion enhances remembrance of neural events past.   Anderson AK, Wais PE and Gabrieli JD.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 1599-1604.

(493) Secondary sex ratios and male lifespan: damaged or culled cohorts.   Catalano R and Bruckner T.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 1639-1643.

(494) Serotonergic neuron diversity: identification of raphe neurons with discharges time-locked to the hippocampal theta rhythm.   Kocsis B, Varga V, Dahan L and Sik A.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 1059-1064.

(495) Neural connections of the posteromedial cortex in the macaque.   Parvizi J, Van Hoesen GW, Buckwalter J and Damasio A.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 1563-1568.

(496) Cortical signatures of noun and verb production.   Shapiro KA, Moo LR and Caramazza A.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 1644-1649.

(497) Gonadal hormone modulation of hippocampal neurogenesis in the adult.   Galea LA, Spritzer MD, Barker JM and Pawluski JL.   2006.   Hippocampus, volume 16, pages 225-232.

(498) Reliability in communication systems and the evolution of altruism.   Zahavi A, in Evolutionary Ecology, pages 253-259.   Stonehouse B and Perrins CM, Editors.   London: Macmillan Press.   1977.

(499) Medullary raphe neurons facilitate brown adipose tissue activation.   Nason MW Jr and Mason P.   2006.   Journal of Neuroscience, volume 26, pages 1190-1198.   The last sentence of the abstract reads: "Thus, both p5HT and non-p5HT OFF cells in the medullary raphe facilitate BAT activation in response to cold challenge or pyrogen." However, the full text article shows that while pain that blocked temperature increases inhibited 19 of 25 OFF cells (76%), it activated 48 of 54 ON cells (88%); that no p5HT cells were recorded during the suppression of BAT (brown adipose tissue) temperature increases by pain; and that the opiate agonist DAMGO activated OFF cells and inhibited ON cells. Consequently, the last sentence of the abstract should read: "Thus, p5HT cells in the medullary raphe facilitate BAT activation in response to cold challenge or pyrogen, while non-p5HT cells, both ON and OFF, modulate BAT suppression in response to noxious stimulation."

(500) Cortico-cerebellar coherence during a precision grip task in the monkey.   Soteropoulos DS and Baker SN.   2006.   Journal of Neurophysiology, volume 95, pages 1194-1206.

(501) Prefrontal cortical projections to longitudinal columns in the midbrain periaqueductal gray in macaque monkeys.   1998.   An X, Bandler R, Ongur D and Price JL.   Journal of Comparative Neurology, volume 401, pages 455-479.

(502) Psychogenic urinary retention in women.   Larson JW, Swenson WM, Utz DC and Steinhilber RM.   1963.   Journal of the American Medical Association, volume 184, pages 697-700.

(503) Abnormal electromyographic activity of the urethral sphincter, voiding dysfunction, and polycystic ovaries: a new syndrome?   Fowler CJ, Christmas TJ, Chapple CR, Parkhouse HF, Kirby RS and Jacobs HS.   1988.   British Medical Journal, volume 297, pages 1436-1438.

(504) The cause and natural history of isolated urinary retention in young women.   Swinn MJ, Wiseman OJ, Lowe E and Fowler CJ.   2002.   Journal of Urology, volume 167, pages 151-156.

(505) Urodynamic study of women in urinary retention treated with sacral neuromodulation.   DasGupta R and Fowler CJ.   2004.   Journal of Urology, volume 171, pages 1161-1164.

(506) Tonic and phasic respiratory drives to human genioglossus motoneurons during breathing.   Saboisky JP, Butler JE, Fogel RB, Taylor JL, Trinder JA, White DP and Gandevia SC.   2006.   Journal of Neurophysiology, volume 95, pages 2213-2221.

(507) The role of conditioning and verbal expectancy in the placebo response.   Voudouris NJ, Peck CL and Coleman G.   1990.   Pain, volume 43, pages 121-128.

(508) Classical conditioning and the placebo effect.   Montgomery GH and Kirsch I.   1997.   Pain, volume 72, pages 107-113.

(509) Introducing a placebo needle into acupuncture research.   Streitberger K and Kleinhenz J.   1998.   The Lancet, volume 352, pages 364-365.

(510) The placebo needle, is it a valid and convincing placebo for use in acupuncture trials? A randomised, single-blind, cross-over pilot trial.   White P, Lewith G, Hopwood V and Prescott P.   2003.   Pain, volume 106, pages 401-409.

(511) Working memory and acquisition of implicit knowledge by imagery training without actual task performance.   Helene AF and Xavier GF.   2006.   Neuroscience, volume 139, pages 401-413.

(512) Differential limbic-cortical correlates of sadness and anxiety in healthy subjects: implications for affective disorders.   Liotti M, Mayberg HS, Brannan SK, McGinnis S, Jerabeck P and Fox PT.   2000.   Biological Psychiatry, volume 48, pages 30-42.

(513) Direct recording of theta oscillations in primate prefrontal and anterior cingulate cortices.   Tsujimoto T, Shimazu H and Isomura Y.   2006.   Journal of Neurophysiology, volume 95, pages 2987-3000.

(514) Dorsolateral prefrontal cortex promotes long-term memory formation through its role in working memory organization.   Blumenfeld RS and Ranganath C.   2006.   Journal of Neuroscience, volume 26, pages 916-925.

(515) "Microsmatic humans" revisited: the generation and perception of chemical signals.   Schaal B and Porter RH, in Advances in the Study of Behavior, volume 20, pages 135-199.   Slater PJB, Rosenblatt JS, Beer C and Milinski M, Editors.   Academic Press, Inc.   Harcourt Brace Jovanovich, Publishers.   San Diego, New York, Boston, London, Sydney, Tokyo and Toronto.   1991.

(516) Homosexuality in the ten-spined stickleback (Pygosteus Pungitius L.)   Morris D.   1952.   Behaviour. An International Journal of Comparative Ethology, volume IV, pages 233-261.

(517) "Displacement reactions" in the three-spined stickleback.   Tinbergen NA and Van Iersel JJA.   1948.   Behaviour. An International Journal of Comparative Ethology, volume I, pages 56-63.

(518) "Derived" activities: their causation, biological significance, origin, and emancipation during evolution.   Tinbergen N.   1952.   The Quarterly Review of Biology, volume 27, pages 1-32.

(519) Some displacement activities of the black-headed gull.   Moynihan M.   1953.   Behaviour. An International Journal of Comparative Ethology, volume V, pages 58-60.

(520) The mechanism of an instinctive control system: a hypothesis.   Hayes JS, Russell WMS, Hayes C and Kohsen A.   1954.   Behaviour. An International Journal of Comparative Ethology, volume IV, pages 85-119.

(521) The functional neuroanatomy of working memory: contributions of human brain lesion studies.   Muller NG and Knight RT.   2006.   Neuroscience, volume 139, pages 51-58.

(522) Estimators of the precision of stereological estimates: an example based on the CA1 pyramidal cell layer of rats.   Slomianka L and West MJ.   2005.   Neuroscience, volume 136, pages 757-767.

(523) Preoptic glutamate facilitates male sexual behavior.   Dominguez JM, Gil M and Hull EM.   2006.   Journal of Neuroscience, volume 26, pages 1699-1703.

(524a) Prefrontal and parietal contributions to spatial working memory.   Curtis CE.   2006.   Neuroscience, volume 139, pages 173-180.

(524b) Selection and maintenance of saccade goals in the human frontal eye fields.   Curtis CE and D'Esposito M.   2006.   Journal of Neurophysiology, volume 95, pages 3923-3927.

(525) Unique, common, and interacting cortical correlates of thirst and pain.   Farrell MJ, Egan GF, Zamarripa F, Shade R, Blair-West J, Fox P and Denton DA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 2416-2421.

(526) A default mode of brain function.   Raichle ME, MacLeod AM, Snyder AZ, Powers WJ, Gusnard DA and Shulman GL.   2001.   Proceedings of the National Academy of Sciences of the United States of America, volume 98, pages 676-682.   According to the abstract, the oxygen extraction fraction is defined as "...the ratio of oxygen used by the brain to oxygen delivered by flowing blood...". According to the main text, "...The relationship of oxygen delivery to oxygen utilization can be measured quantitatively in the human brain...This measurement is usually referred to as the oxygen extraction fraction...". So, which is the numerator and which is the denominator in this fraction?

(527) Regional brain metabolism during auditory hallucinations in chronic schizophrenia.   Cleghorn JM, Garnett ES Nahmias C, Brown GM, Kaplan RD, Szechtman H, Szechtman B, Franco S, Dermer SW and Cook P.   1990.   British Journal of Psychiatry, volume 157, pages 562-570.

(528) Cognitive and emotional influences in anterior cingulate cortex.   Bush G, Luu P and Posner MI.   2000.   Trends in Cognitive Sciences, volume 4, pages 215-222.

(529) Lateralized cognitive processes and lateralized task control in the human brain.   Stephan KE, Marshall JC, Friston KJ, Rowe JB, Ritzl A, Zilles K and Fink GR.   2003.   Science, volume 301, pages 384-386.

(530) Toward a brain map of auditory hallucinations.   Cleghorn JM, Franco S, Szechtman B, Kaplan RD, Szechtman H, Brown GM, Nahmias C and Garnett ES.   1992.   American Journal of Psychiatry, volume 149, pages 1062-1069.

(531) Where the imaginal appears real: a positron emision tomography study of auditory hallucinations.   Szechtman H, Woody E, Bowers KS and Nahmias C.   1998.   Proceedings of the National Academy of Sciences of the United States of America, volume 95, pages 1956-1960.

(532) Mapping auditory hallucinations in schizophrenia using functional magnetic resonance imaging.   Shergill SS, Brammer MJ, Williams SC, Murray RM and McGuire PK.   2000.   Archives of General Psychiatry, volume 57, pages 1033-1038.

(533) Nanomechanics of the subtectorial space caused by electromechanics of cochlear outer hair cells.   Nowotny M and Gummer AW.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 2120-2125.

(534) Influence of spatial information on responses of tonically active neurons in the monkey striatum.   Ravel S, Sardo P, Legallet E and Apicella P.   2006.   Journal of Neurophysiology, volume 95, pages 2975-2986.

(535) Block of inferior olive gap junctional coupling decreases Purkinje cell complex spike synchrony and rhythmicity.   Blenkinsop TA and Lang EJ.   2006.   Journal of Neuroscience, volume 26, pages 1739-1748.

(536) Bidirectional connections of the medial amygdaloid nuclus in the Syrian hamster brain: simultaneous anterograde and retrograde tract tracing.   Coolen LM and Wood RI.   1998.   Journal of Comparative Neurology, volume 399, pages 189-209.

(537) c-fos expession in vomeronasal pathways of mated or pheromone-stimulated male golden hamsters: contributions from vomeronasal sensory input and expression related to mating performance.   Fernandez-Fewell GD and Meredith M.   1994.   Journal of Neuroscience, volume 14, pages 3643-3654.

(538) Neural control of ejaculation.   Coolen LM.   2005.   Journal of Comparative Neurology, volume 493, pages 39-45.

(539) Simultaneous release of glutamate and acetylcholine from single magnocellular "cholinergic" basal forebrain neurons.   Allen TG, Abogadie FC and Brown DA.   2006.   Journal of Neuroscience, volume 26, pages 1588-1595.

(540) Dissociating the role of ventral and dorsal premotor cortex in precision grasping.   Davare M, Andres M, Cosnard G, Thonnard JL and Olivier E.   2006.   Journal of Neuroscience, volume 26, pages 2260-2268.

(541) Repetitive transcranial magnetic stimulation-induced changes in sensorimotor coupling parallel improvements of somatosensation in humans.   Pleger B, Blankenburg F, Bestmann S, Ruff CC, Wiech K, Stephan KE, Friston KJ and Dolan RJ.   2006.   Journal of Neuroscience, volume 26, pages 1945-1952.

(542) Differences in the effects of medial and lateral preoptic lesions on thermoregulation and sleep in rats.   Srividya R, Mallick HN and Kumar VM.   2006.   Neuroscience, volume 139, pages 853-864.

(543) The subfornical organ: a central target for circulating feeding signals.   Pulman KJ, Fry WM, Cottrell GT and Ferguson AV.   2006.   Journal of Neuroscience, volume 26, pages 2022-2030.

(544) Neural circuitry underlying rule use in humans and nonhuman primates.   Bunge SA, Wallis JD, Parker A, Brass M, Crone EA, Hoshi E and Sakai K.   2005.   Journal of Neuroscience, volume 22, pages 10347-10350.

(545) Feedforward inhibition regulates perirhinal transmission of neocortical inputs to the entorhinal cortex: ultrastructural study in guinea pigs.   Pinto A, Fuentes C and Pare D.   2006.   Journal of Comparative Neurology, volume 495, pages 722-734.

(546) Localization of the neurons active during paradoxical (REM) sleep and projecting to the locus coeruleus noradrenergic neurons in the rat.   Verret L, Fort P, Gervasoni D, Leger L and Luppi PH.   2006.   Journal of Comparative Neurology, volume 495, pages 573-586.

(547) Intracortical inhibition during volitional inhibition of prepared action.   Coxon JP, Stinear CM and Byblow WD.   2006.   Journal of Neurophysiology, volume 95, pages 3371-3383.

(548) Goal representation in human anterior intraparietal sulcus.   Hamilton AF and Grafton ST.   2006.   Journal of Neuroscience, volume 26, pages 1133-1137.

(549) Women use voice parameters to assess men's charactristics.   Bruckert L, Lienard JS, Lacroix A, Kreutzer M and Leboucher G.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 83-89.

(550) Transitions to asexuality result in excess amino acid substitutions.   Paland S and Lynch M.   2006.   Science, volume 311, pages 990-992.    Editorial. Sex pays off.   2006.   Science, volume 311, pages 913-915.    Comment. Why sex?   Nielsen R.   2006.   Science, volume 311, pages 960-961.    Comment. Comment on "Transitions to asexuality result in excess amino acid substitutions".   Butlin R.   2006.   Science, volume 313, page 1389.    Author reply, page 1389.

(551) The Social Life of Monkeys and Apes.   Zuckerman S.   Kegan Paul, Trench, Trubner and Co. Ltd.   London, Broadway House: 68-74 Carter Lane, E.C.   1932.

(552) Causal reasoning in rats.   Blaisdell AP, Sawa K, Leising KJ and Waldmann MR.   2006.   Science, volume 311, pages 1020-1022.    Editorial. Rats are smarter than we think.   2006.   Science, volume 311, page 915.   The more significant, but less explored, difference in experiment 1 was between Condition Intervene-N and Condition Intervene-T, P<0.01, probably a reflection of the use of simultaneity in group N but not in group T, such that the strength of association was greater in group N than in group T, and thus less likely to be disrupted by the interventions. Condition Observe-N was greater than Condition Observe-T, but not significantly so, and this trend is consistent with models of working memory.

(553) On making the right choice: the Deliberation-Without-Attention effect.   Dijksterhuis A, Bos MW, Nordgren LF and van Baaren RB.   2006.   Science, volume 311, pages 1005-1007.    Editorial. Don't think too much.   2006.   Science, volume 311, page 915.    Comment. Tough decision? Don't sweat it.   Miller G.   2006.   Science, volume 311, page 935.

(554) Autonomic neurons in the spinal cord of the Rhesus monkey: a correlation of the findings of cytoarchitectonics and sympathectomy with fiber degeneration following dorsal rhizotomy.   Petras JM and Cummings JF.   1972.   Journal of Comparative Neurology, volume 146, pages 189-218.

(555a) Cortical connections of the auditory cortex in marmoset monkeys: core and medial belt regions.   De La Mothe LA, Blumell S, Kajikawa Y and Hackett TA.   2006.   Journal of Comparative Neurology, volume 496, pages 27-71.

(555b) Thalamic connections of the auditory cortex in marmoset monkeys: core and medial belt regions.   De La Mothe LA, Blumell S, Kajikawa Y and Hackett TA.   2006.   Journal of Comparative Neurology, volume 496, pages 72-96.

(556) Single-axon tracing study of corticostriatal projections arising from primary motor cortex in primates.   Parent M and Parent A.   2006.   Journal of Comparative Neurology, volume 496, pages 202-213.

(557) An optimal brain can be composed of conflicting agents.   Livnat A and Pippenger N.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 3198-3202.

(558) Between-subject transfer of emotional information evokes specific pattern of amygdala activation.   Knapska E, Nikolaev E, Boguszewski P, Walasek G, Blaszczyk J, Kaczmarek L and Werka T.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 3858-3862.

(559) Neural correlates of tic generation in Tourette syndrome: an event-related functional MRI study.   Bohlhalter S, Goldfine A, Matteson S, Garraux G, Hanakawa T, Kansaku K, Wurzman R and Hallett M.   2006.   Brain, volume 129, pages 2029-2037.

(560) Asymmetries of the planum temporale and Heschl's gyrus: relationship to language lateralization.   Dorsaint-Pierre R, Penhune VB, Watkins KE, Neelin P, Lerch JP, Bouffard M and Zatorre RJ.   2006.   Brain, volume 129, pages 1164-1176.

(561) Directly reactivated, but not indirectly reactivated, memories undergo reconsolidation in the amygdala.   Debiec J, Doyere V, Nader K and Ledoux JE.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 3428-3433.   There is no reference to the amygdala in the abstract.

(562) Neurochemical modulation of response inhibition and probabilistic learning in humans.   Chamberlain SR, Müller U, Blackwell AD, Clark L, Robbins TW and Sahakian BJ.   2006.   Science, volume 311, pages 861-863.

(563) On the ability to inhibit simple and choice reaction time responses: a model and a method.   Logan GD, Cowan WB and Davis KA.   1984.   Journal of Experimental Psychology. Human Perception and Performance, volume 10, pages 276-291.

(564) A role for the periaqueductal gray in switching adaptive behavioral responses.   Sukikara MH. Mota-Ortiz SR, Baldo MV, Felicio LF and Canteras NS.   2006.   Journal of Neuroscience, volume 26, pages 2583-2589.

(565) The evolution and functions of laughter and humor: a synthetic approach.   Gervais M and Wilson DS.   2005.   The Quarterly Review of Biology, volume 80, pages 395-430.   With reference to working memory, emotional laughter, eponymously referred to as Duchenne laughter (see this reference, page 396, and reference (286), page 2122), may occur some time after the humorous stimulus, because working memory has enabled reverberation of the stimulus until there has been time for a reflective chuckle. Self-generated and emotionless laughter may be associated with stimuli by chance, or by personal meaning, as in the wry, sardonic sigh.

(566) Prior specification in Bayesian statistics: three cautionary tales.   Van Dongen S.   2006.   Journal of Theoretical Biology, volume 242, pages 90-100.

(567) The role of brain stem-spinal systems in genital stimulation: induced inhibition of sensory and motor responses to noxious stimulation.   Komisaruk BR, in Brain Stem Control of Spinal Mechanisms, pages 493-508.   Sjölund B and Björklund A, Editors.   Elsevier Biomedical Press.   Amsterdam, New York, London.   1982.

(568) Inhibitory control from the brain stem of transmission from primary afferents to motoneurons, primary afferent terminals and ascending pathways.   Lundberg A, in Brain Stem Control of Spinal Mechanisms, pages 179-224.   Sjölund B and Björklund A, Editors.   Elsevier Biomedical Press.   Amsterdam, New York, London.   1982.

(569) On the function of recurrent inhibition in the spinal cord.   Hultborn H, Lindstrom S and Wigstrom H.   1979.   Experimental Brain Research, volume 37, pages 399-403.

(570) Parietal area 5 and the initiation of self-timed movements versus simple reactions.   Maimon G and Assad JA.   2006.   Journal of Neuroscience, volume 126, pages 2487-2498.

(571) Warning displays in spiny animals: one (more) evolutionary route to aposematism.   Speed MP and Ruxton GD.   2005.   Evolution. International Journal of Organic Evolution, volume 59, pages 2499-2508.

(572) The effect of intraspecific sample size on type I and type II error rates in comparative studies.   Harmon LJ and Losos JB.   2005.   Evolution. International Journal of Organic Evolution, volume 59, pages 2705-2710.

(573) Cortical and subcortical contributions to Stop signal response inhibition: role of the subthalamic nucleus.   Aron AR and Poldrack RA.   2006.   Journal of Neuroscience, volume 26, pages 2424-2433.

(574) Experiencing oneself vs another person as being the cause of an action: the neural correlates of the experience of agency.   Farrer C and Frith CD.   2002.   Neuroimage, volume 15, pages 596-603.

(575) Both social and ecological factors predict ungulate brain size.   Shultz S and Dunbar RI.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 207-215.

(576) Accepting loss: the temporal limits of reciprocity in brown capuchin monkeys.   Ramseyer A, Pele M, Dufour V, Chauvin C and Thierry B.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 179-184.

(577) Endogenous timing in competitive interactions among relatives.   Cant MA and Shen SF.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 171-178.

(578) Inbreeding depression and the evolution of dispersal rates: a multilocus model.   Roze D and Rousset F.   2005.   The American Naturalist, volume 166, pages 708-721.

(579) Group living and inbreeding depression in a subsocial spider.   Aviles L and Bukowski TC.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 157-163.

(580) How can automimicry persist when predators can preferentially consume undefended mimics?   Ruxton GD and Speed MP.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 373-378.

(581) Facial appearance is a cue to oestrogen levels in women.   Smith MJ, Perrett DI, Jones BC, Cornwell RE, Moore FR, Feinberg DR, Boothroyd LG, Durrani SJ, Stirrat MR, Whiten S, Pitman RM and Hillier SG.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 135-140.

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(706) Stress-induced alternative splicing of acetylcholinesterase results in enhanced fear memory and long-term potentiation.   Nijholt I, Farchi N, Kye M, Sklan EH, Shoham S, Verbeure B, Owen D, Hochner B, Spiess J, Soreq H and Blank T.   2004.   Molecular Psychiatry, volume 9, pages 174-183.

(707) Cellular and molecular neuropathology of the parahippocampal region in schizophrenia.   Arnold SE.   2000.   Annals of the New York Academy of Sciences, volume 911, pages 275-292.

(708) Abnormal cholecystokinin mRNA levels in entorhinal cortex of schizophrenics.   Bachus SE, Hyde TM, Herman MM, Egan MF and Kleinman JE.   1997.   Journal of Psychiatric Research, volume 31, pages 233-256.

(709) Beyond affect: a role for genetic variation of the serotonin transporter in neural activation during a cognitive attention task.   Canli T, Omura K, Haas BW, Fallgatter A, Constable RT and Lesch KP.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 12224.12229.

(710) Character displacement as the "best of a bad situation": fitness trade-offs resulting from selection to minimize resource and mate competition.   Pfennig KS and Pfennig DW.   2005.   Evolution. International Journal of Organic Evolution, volume 59, pages 2200-2208.

(711) Cooperation through interdependence.   Roberts G.   2005.   Animal Behaviour, volume 70, pages 901-908.

(712) Sleeping under the risk of predation.   Lima SL, Rattenborg NC, Lesku JK and Amlaner CJ.   2005.   Animal Behaviour, volume 70, pages 723-736.

(713) Canalization of development and the inheritance of acquired characters.   Waddington CH.   1942.   Nature, volume 150, pages 563-565.

(714) Micturition and the soul.   Holstege G.   2005.   Journal of Comparative Neurology, volume 493, pages 15-20.

(715) Self-sustained activity in a small-world network of excitable neurons.   Roxin A, Riecke H and Solla SA.   2004.   Physical Review Letters, volume 92, page 198101.

(716) Parental antagonism, related asymmetries, and genomic imprinting.   Haig D.   1997.   Proceedings. Biological Sciences / The Royal Society, volume 264, pages 1657-1662.

(717) What good is genomic imprinting: the function of parent-specific gene expression.   Wilkins JF and Haig D.   2003.   Nature Review Genetics, volume 4, pages 359-368.

(718) Inbreeding, maternal care, and genomic imprinting.   Wilkins JF and Haig D.   2003.   Journal of Theoretical Biology, volume 221, pages 559-564.   The use of the verb "lavish" to describe the quality of care given by female mice to their offspring is overstatement from the perspective of a mouse, and is followed predictably by a preposterous genetic anthropomorphism "...disagreement between the maternally and paternally derived genomes of mothers...".

(719) What's in it for me? Self-regard precludes altruism and spite in chimpanzees.   Jensen K, Hare B, Call J and Tomasello M.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1013-1021.

(720) Outbreeding selects for spiteful cytoplasmic elements.   Engelstadter J and Charlat S.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 923-929.

(721) Electrophysiological properties of cholinergic and noncholinergic neurons in the ventral pallidal region of the nucleus basalis in rat brain slices.   Bengtson CP and Osborne PB.   2000.   Journal of Neurophysiology, volume 83, pages 2649-2660.

(722) Impaired recognition of anger following damage to the ventral striatum.   Calder AJ, Keane J, Lawrence AD and Manes F.   2004.   Brain, volume 127, pages 1958-1969.

(723) Self-imposed silence: parental antagonism and the evolution of X-chromosome inactivation.   Haig D.   2006.   Evolution. International Journal of Organic Evolution, volume 60, pages 440-447.

(724) Gene expression profile for schizophrenia: discrete neuron transcription patterns in the entorhinal cortex.   Hemby SE, Ginsberg SD, Brunk B, Arnold SE, Trojanowski JO and Eberwine JH.   2002.   Archives of General Psychiatry, volume 59, pages 631-640.

(725) Sex ratios under asymmetrical local mate competition: theory and a test with parasitoid wasps.   Shuker DM, Pen I, Duncan AB, Reece SE and West SA.   2005.   The American Naturalist, volume 166, pages 301-316.

(726) A large family of ancient repeat elements in the human genome is under strong selection.   Kamal M, Xie X and Lander ES.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 2740-2745.

(727) The dreaming sleep stage: a new neurobiological model of schizophrenia?   Gottesmann C.   2006.   Neuroscience, volume 140, pages 1105-1115.   The elliptical final sentence of the abstract reflects the elliptical model, which does not acknowledge differences between sleep and schizophrenia, such as level of consciousness and delusions.

(728) Entorhinal cortex pre-alpha cell clusters in schizophrenia: quantitative evidence of a developmental abnormality.   Falkai P, Schneider-Axmann T and Honer WG.   2000.   Biological Psychiatry, volume 47, pages 937-943.

(729) Content- and task- specific dissociations of frontal activity during maintenance and manipulation in visual working memory.   Mohr HM, Goebel R and Linden DE.   2006.   Journal of Neuroscience, volume 26, pages 4465-4471.

(730) Perceptual knowledge retrieval activates sensory brain regions.   Goldberg RF, Perfetti CA and Schneider W.   2006.   Journal of Neuroscience, volume 26, pages 4917-4921.

(731) Alternative designs and the evolution of functional diversity.   Marks CO and Lechowicz MJ.   2006.   The American Naturalist, volume 167, pages 55-66.

(732) Evolution and maintenance of the environmental component of the phenotypic variance: benefit of plastic traits under changing environments.   Zhang XS.   2005.   The American Naturalist, volume 166, pages 569-580.

(733) Self-recognition, color signals, and cycles of greenbeard mutualism and altruism.   Sinervo B, Chaine A, Clobert J, Calsbeek R, Hazard L, Lancaster L, McAdam AG, Alonzo S, Corrigan G and Hochberg ME.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 7372-7377.

(734) Sexual differentiation of central vasopressin and vasotocin systems in vertebrates: different mechanisms, similar endpoints.   De Vries GJ and Panzica GC.   2005.   Neuroscience, volume 138, pages 947-955.

(735) Effect of varying epistasis on the evolution of recombination.   Kouyos RD, Otto SP and Bonhoeffer S.   2006.   Genetics, volume 173, pages 589-597.

(736) Plasticity in the human central nervous system.   Cooke SF and Bliss TV.   2006.   Brain, volume 129, pages 1659-1673.

(737) Cortical inhibitory neurons and schizophrenia.   Lewis DA, Hashimoto T and Volk DW.   2005.   Nature Reviews. Neuroscience, volume 6, pages 312-324.

(738) Cytokine modulation of defensive rage behavior in the cat: role of GABA(a) and interleukin-2 receptors in the medial hypothalamus.   Bhatt S, Zalcman S, Hassanain M and Siegel A.   2005.   Neuroscience, volume 133, pages 17-28.

(739) Structural characterization of a hypothalamic visceromotor pattern generator network.   Thompson RH and Swanson LW.   2003.   Brain Research. Brain Research Reviews, volume 41, pages 153-202.

(740) Cellular composition and cytoarchitecture of the adult human subventricular zone: a niche of neural stem cells.   Quinones-Hinojosa A, Sanai N, Soriano-Navarro M, Gonzalez-Perez O, Mirzadeh Z, Gil-Perotin S, Romero-Rodriguez R, Berger MS, Garcia-Verdugo JM and Alvarez-Buylla A.   2006.   Journal of Comparative Neurology, volume 494, pages 415-434.

(741) Endocrine self and gut non-self intersect in the pancreatic lymph nodes.   Turley SJ, Lee JW, Dutton-Swain N, Mathis D and Benoist C.   2005.    Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 17729-17733.

(742) Gating and habituation of the startle reflex in schizophrenic patients.   Braff DL, Grillon C and Geyer MA.   1992.   Archives of General Psychiatry, volume 49, pages 206-215.

(743) Sentisization and habituation of the acoustic startle reflex in patients with schizophrenia.   Meincke U, Light GA, Geyer MA, Braff DL and Gouzoulis-Mayfrank E.   2004.   Psychiatry Research, volume 126, pages 51-61.

(744) The structures of letters and symbols throughout human history are selected to match those found in objects in natural scenes.   Changizi MA, Zhang O, Ye H and Shimojo S.   2006.   The American Naturalist, volume 167(5), pages E117-E139.

(745) Context-dependent discrimination and the evolution of mimicry.   Holen OH and Johnstone RA.   2006.   The American Naturalist, volume 167, pages 377-389.

(746) Testing the relationship between morphological and molecular rates of change among phylogenies.   Bromham L, Woolfit M, Lee MS and Rambaut A.   2002.   Evolution. International Journal of Organic Evolution, volume 56, pages 1921-1930.

(747) Neutral theory, phylogenies, and the relationship between phenotypic change and evolutionary rates.   Davies TJ and Savolainen V.   2006.   Evolution. International Journal of Organic Evolution, volume 60, pages 476-483.

(748) Attentional modulation of thalamic reticular neurons.   McAlonan K, Cavanaugh J and Wurtz RH.   2006.   Journal of Neuroscience, volume 26, pages 4444-4450.

(749) Amygdala and ventromedial prefrontal cortex are inversely coupled during regulation of negative affect and predict the diurnal pattern of cortisol secretion among older adults.    Urry HL, van Reekum CM, Johnstone T, Kalin NH, Thurow ME, Schaefer HS, Jackson CA, Frye CJ, Greischar LL, Alexander AL and Davidson RJ.   2006.   Journal of Neuroscience, volume 26, pages 4415-4425.

(750) Reverse replay of behavioural sequences in hippocampal place cells during the awake state.   Foster DJ and Wilson MA.   2006.   Nature, volume 440, pages 680-683.

(751) Structured demes and the evolution of group-advantageous traits.   Wilson DS.   1977.   The American Naturalist, volume 111, pages 157-185.

(752) Human QKI, a potential regulator of mRNA expression of human oligodendrocyte-related genes involved in schizophrenia.   Aberg K, Saetre P, Jareborg N and Jazin E.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 7482-7487.

(753) Sexual reproduction reshapes the genetic architecture of digital organisms.   Misevic D, Ofria C and Lenski RE.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 457-464.

(754) Colocalization of corticotropin-releasing hormone and oestrogen receptor-alpha in the paraventricular nucleus of the hypothalamus in mood disorders.   Bao AM, Hestiantoro A, Van Someren EJ, Swaab DF and Zhou JN.   2005.   Brain, volume 128, pages 1301-1313.

(755) Growth hormone is produced within the hippocampus where it responds to age, sex, and stress.   Donahue CP, Kosik KS and Shors TJ.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 6031-6036.   This appears to be an inference, based on the presence of GH mRNA and GH protein, as distinct from GH itself.   

(756) The entorhinal cortex in first-episode psychotic disorders: a structural magnetic resonance imaging study.   Prasad KM, Patel AR, Muddasani S, Sweeney J and Keshavan MS.   2004.   American Journal of Psychiatry, volume 161, pages 1612-1619.   The first sentence of the conclusion of a tautology, because, by definition, first episodes are not confounded by chronicity, and neuroleptic-naive psychotic disorders cannot be confounded by antipsychotic treatment. What is meant is that, because smaller entorhinal cortex volumes have been observed in first-episode, neuroleptic-naive psychotic disorders, they may not reflect chronicity or treatment when seen in later, treated episodes.

(757) Individual differences in reward drive predict neural responses to images of food.   Beaver JD, Lawrence AD, van Ditzhuijzen J, Davis MH, Woods A and Calder AJ.   2006.   Journal of Neuroscience, volume 26, pages 5160-5166.

(758) The dopaminergic midbrain participates in human episodic memory formation: evidence from genetic imaging.   Schott BH, Seidenbecher CI, Fenker DB, Lauer CJ, Bunzeck N, Bernstein HG, Tischmeyer W, Gundelfinger ED, Heinze HJ and Duzel E.   2006.   Journal of Neuroscience, volume 26, pages 1407-1417.

(759) Metabolic indices shift in the hypothalamic-neurohypophysial system during lactation: implications for interpreting their relationship with neuronal activity.   Uribe-Querol E, Martinez-Martinez E, Tapia-Roderiguez M, Hernandez LR, Toscano-Marquez B, Padilla P and Gutierrez-Ospina G.   2005.   Journal of Neuroscience, volume 134, pages 1217-1222.

(760) Effects of dopamine depletion on visual sensitivity of Zebrafish.   Lei L and Dowling JE.   2000.   Journal of Neuroscience, volume 20, pages 1893-1903.

(761) Extended habit training reduces dopamine mediation of appetitive response expression.   Choi WY, Balsam PD and Horvitz JC.   2005.   Journal of Neuroscience, volume 25, pages 6729-6733.

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(765) Abnormal neural synchrony in schizophrenia.   Spencer KM, Nestor PG, Niznikiewicz MA, Salisbury DF, Shenton ME and McCarley RW.   2003.   Journal of Neuroscience, volume 23, pages 7407-7411.

(766) Neural synchrony indexes disordered perception and cognition in schizophrenia.   Spencer KM, Nestor PG, Perlmutter R, Niznikiewicz MA, Klump MC, Frumin M, Shenton ME and McCarley RW.   2004.   Proceedings of the National Academy of Sciences of the United States of America, volume 101, pages 17288-17293.

(767) Hierarchical structures induce long-range dynamical correlations in written texts.   Alvarez-Lacalle E, Dorow B, Eckmann JP and Moses E.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 7956-7961.

(768) Hotspots for copy number variation in chimpanzees and humans.   Perry GH, Tchinda J, McGrath SD, Zhang J, Picker SR, Caceres AM, Iafrate AJ, Tyler-Smith C, Scherer SW, Eichler EE, Stone AC and Lee C.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8006-8011.

(769) Failing to deactivate: resting functional abnormalities in autism.   Kennedy DP, Redcay E and Courchesne E.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8275-8280.   

(770) Direct and fast detection of neuronal activation in the human brain with diffusion MRI.   Le Bihan D, Urayama SI, Aso T, Hanakawa T and Fukuyama H.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8263-8268.

(771) Binding crossmodal object features in perirhinal cortex.   Taylor KI, Moss HE, Stamatakis EA and Tyler LK.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8239-8244.

(772) Exercise training differentially affects intrinsic excitability of autonomic and neuroendocrine neurons in the hypothalamic paraventricular nucleus.   Jackson K, Vieira Silva HM, Zhang W, Michelini LC and Stern JE.   2005.   Journal of Neurophysiology, volume 94, pages 3211-3220.

(773) Involvement of the bed nucleus of the stria terminalis activated by the central nucleus of the amygdala in the negative affective component of morphine withdrawal in rats.   Nakagawa T, Yamamoto R, Fujio M, Suzuki Y, Minami M, Satoh M and Kaneko S.   2005.   Neuroscience, volume 134, pages 9-19.

(774) Pheromones and Animal Behaviour. Communication by Smell and Taste.   Wyatt TD.   Cambridge University Press, Cambridge.   2003.

(775) Brain oxytocin correlates with maternal aggression: link to anxiety.   Bosch OJ, Meddle SL, Beiderbeck DI, Douglas AJ and Neumann ID.   2005.   Journal of Neuroscience, volume 25, pages 6807-6815.

(776) Comprehensive mutation identification in an evolved bacterial cooperator and its cheating ancestor.   Velicer GJ, Raddatz G, Keller H, Deiss S, Lanz C, Dinkelacker I and Schuster SC.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8107-8112.

(777) Brain response to putative pheromones in lesbian women.   Berglund H, Lindstrom P and Savic I.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8269-8274.

(778) Tissue plasminogen activator in the bed nucleus of stria terminalis regulates acoustic startle.   Matys T, Pawlak R and Strickland S.   2005.   Neuroscience, volume 135, pages 715-722.

(779) Urocortin 1-containing neurons in the human Edinger-Westphal nucleus.   Ryabinin AE, Tsivkovskaia NO and Ryabanin SA.   2005.   Neuroscience, volume 134, pages 1317-1323.

(780) Identification of wake-active dopaminergic neurons in the ventral periaqueductal gray matter.   Lu J, Jhou TC and Saper CB.   2006.   Journal of Neuroscience, volume 26, pages 193-202.   The chosen index of dopamine cell activity did not appear until after 30 minutes of forced wakefulness in rats. Why did it take so long if it was an index of arousal? Was it because of the rats' movement in response to forced wakefulness?

(781) Geographical variation in selection, from phenotypes to molecules.   Kelly JK.   2006.   The American Naturalist, volume 167, pages 481-495.

(782) Schizophrenics show spatial working memory deficits.   Park S and Holzman PS.   1992.   Archives of General Psychiatry, volume 49, pages 975-982.

(783) Role of early experience in ant enslavement: a comparative analysis of a host and non-host species.   Blatrix R and Sermage C.   2005.   Frontiers in Zoology, Aug 2;2:13.

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(785) Spontaneous activity and properties of two types of principal neurons from the ventral tegmental area of rat.   Koyama S, Kanemitsu Y and Weight FF.   2005.   Journal of Neurophysiology, volume 93, pages 3282-3293.

(786) A bottom-up approach to gene regulation.   Guido NJ, Wang X, Adalsteinsson, McMillen D, Hasty J, Cantor CR, Elston TC and Collins JJ.   2006.   Nature, volume 439, pages 856-860.

(787) The primate amygdala represents the positive and negative value of visual stimuli during learning.   Paton JJ, Belova MA, Morrison SE and Salzman CD.   2006.   Nature, volume 439, pages 865-870.

(788) Sexual reproduction selects for robustness and negative epistasis in artificial gene networks.   Azevedo RB, Lohaus R, Srinivasan S, Dang KK and Burch CL.   2006.   Nature, volume 440, pages 87-90.

(789) RNAi-mediated gene silencing in non-human primates.   Zimmermann TS, Lee AC, Akinc A, Bramlage B, Bumcrot D, Fedoruk MN, Harborth J, Heyes JA, Jeffs LB, John M, Judge AD, Lam K, McClintock K, Nechev LV, Palmer LR, Racie T, Rohl I, Seiffert S, Shanmugam S, Sood V, Soutschek J, Toudjarska I, Wheat AJ, Yaworski E, Zedalis W, Koteliansky V, Manoharan M, Vornlocher HP and MacLachlan I.   2006.   Nature, volume 441, pages 111-114.

(790) Altruism through beard chromodynamics.   Jansen VA and van Baalen M.   2006.   Nature, volume 440, pages 663-666.

(791) Identifying hypothalamic pathways controlling food intake, body weight, and glucose homeostasis.   Elmquist JK, Coppari R, Balthasar M, Ichinose M and Lowell BB.   2005.   Journal of Comparative Neurology, volume 493, pages 63-71.

(792) Local expression of GH and IGF-1 in the hippocampus GH-deficient long-lived mice.   Sun LY, Al-Regaiey K, Masternak MM, Wang J and Bartke A.   2005.   Neurobiology of Aging, volume 26, pages 929-937.   This appears to be an inference, based on the presence of GH protein, as distinct from GH itself.   

(793) Regulation of ovulation by human pheromones.   Stern K and McClintock MK.   1998.   Nature, volume 392, pages 177-179.    Comment. Communication through body odour.   Weller A.   1998.   Nature, volume 392, pages 126-127.    Comment. Pheromones and regulation of ovulation.   Whitten W.   1999.   Nature, volume 401, page 232.    Author reply, pages 232-233.

(794) Psychological state and mood effects of steroidal chemosignals in women and men.   Jacob S and McClintock MK.   2000.   Hormones and Behavior, volume 37, pages 57-78.   

(795) Sustained human chemosignal unconsciously alters brain function.   Jacob S, Kinnunen LH, Metz J, Cooper M and McClintock MK.   2001.   Neuroreport, volume 12, pages 2391-2394.

(796) Parasites as causative agents of human affective disorders? The impact of anti-psychotic, mood-stabilizer and anti-parasite medication on Toxoplasma gondii's ability to alter host behaviour.   Webster JP, Lamberton PH, Donnelly CA and Torrey EF.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1023-1030.

(797) Laminar inputs from dorsal cochlear nucleus and ventral cochlear nucleus to the central nucleus of the inferior colliculus: two patterns of convergence.   Malmierca MS, Saint Marie RL, Merchan MA and Oliver DL.   2005.   Neuroscience, volume 136, pages 883-894.

(798) Theta and gamma oscillations during encoding predict subsequent recall.   Sederberg PB, Kahana MJ, Howard MW, Donner EJ and Madsen JR.   2003.   Journal of Neuroscience, volume 23, pages 10809-10814.

(799) Processes of copy-number change in human DNA: the dynamics of {alpha}-globin gene deletion.   Lam KW and Jeffreys AJ.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8921-8927.

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(801) From lesions to leptin: hypothalamic control of food intake and body weight.   Elmquist JK, Elias CF and Saper CB.   1999.   Neuron, volume 22, pages 221-232.

(802) Differential regulation of metabolic, neuroendocrine and immune function by leptin in humans.   Chan JL, Matarese G, Shetty GK, Raciti P, Kelesidis I, Aufiero D, De Rosa V, Perna F, Fontana S and Mantzoros CS.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8481-8486.

(803) Distributions of two gonadotrophin-releasing hormone receptor types in a cichlid fish suggest functional specialization.   Chen CC and Fernald RD.   2006.   Journal of Comparative Neurology, volume 495, pages 314-323.

(804) Energetics reveals physiologically distinct castes in a eusocial mammal.   Scantlebury M, Speakman JR, Oosthuizen MK, Roper TJ and Bennett NC.   2006.   Nature, volume 440, pages 795-797.

(805) Pharmaco-metabonomic phenotyping and personalized drug treatment.   Clayton TA, Lindon JC, Cloarec O, Antti H, Charuel C, Hanton G, Provost JP, Le Net JL, Baker D, Walley RJ, Everett JR and Nicholson JK.   2006.   Nature, volume 440, pages 1073-1077.

(806) Gene therapy: therapeutic gene causing lymphoma.   Woods NB, Bottero V, Schmidt M, von Kalle C and Verma IM.   2006.   Nature, volume 440, page 1123.

(807) A proposed hypothalamic-thalamic-striatal axis for the integration on energy balance, arousal, and food reward.   Kelley AE, Baldo BA and Pratt WE.   2005.   Journal of Comparative Neurology, volume 493, pages 72-85.

(808) Projections from the subfornical region of the lateral hypothalamic area.   Goto M, Canteras NS, Burns G and Swanson LW.   2005.   Journal of Comparative Neurology, volume 493, pages 412-438.

(809) Absolute rate theories of epigenetic stability.   Walczak AM, Onuchic JN and Wolynes PG.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 18926-18931.

(810) Rank-related maternal effects of androgens on behaviour in wild spotted hyaenas.   Dloniak SM, French JA and Holekamp KE.   2006.   Nature, volume 440, pages 1190-1193.

(811) Chimpanzees are indifferent to the welfare of unrelated group members.   Silk JB, Brosnan SF, Vonk J, Henrich J, Povinelli DJ, Richardson AS, Lambeth SP, Mascaro J and Schapiro SJ.   2005.   Nature, volume 437, pages 1357-1359.    Comment. Animal behaviour: chimpanzee choice and prosociality.   Beninger RJ and Qunisey VL.   2006.   Nature, volume 440:E6; discussion E6.

(812) Future fitness and helping in social queues.   Field J, Cronin A and Bridge C.   2006.   Nature, volume 441, pages 214-217.

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(814) Cortical processing of human somatic and visceral sensation.   Aziz Q, Thompson DG, Ng VWK, Hamdy S, Sarkar S, Brammer MJ, Bullmore ET, Hobson A, Tracey I, Gregory L, Simmons A and Williams SCR.   2000.   Journal of Neuroscience, volume 20, pages 2657-2663.

(815) Opposite effects of noradrenaline and acetylcholine upon hypocretin/orexin versus melanin concentrating hormone neurons in rat hypothalamic slices.   Bayer L, Eggermann E, Serafin M, Grivel J, Machard D, Muhlethaler M and Jones BE.   2005.   Neuroscience, volume 130, pages 807-811.

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(817) Resource competition and social conflict in experimental populations of yeast.   Maclean RC and Gudelj I.   2006.   Nature, volume 441, pages 498-501.

(818) Human dynamics: Darwin and Einstein corrrespondence patterns.   Oliveira JG and Barabasi AL.   2005.   Nature, volume 437, page 1251.    Comment. Correspondence patterns: mechanisms and models of human dynamics.   Kentsis A.   2006.   Nature, volume 441: E5.    Reply. Correspondence patterns: mechanisms and models of human dynamics.   Oliveira JG and Barabasi AL.   2006.   Nature, volume 441: E5-6.

(819) A simple rule for the evolution of cooperation on graphs and social networks.   Ohtsuki H, Hauert C, Lieberman E and Nowak MA.   2006.   Nature, volume 441, pages 502-505.

(820) Central structures necessary and sufficient for ingestive and glycemic responses to Urocortin I administration.   Daniels D, Markison S, Grill HJ and Kaplan JM.   2004.   Journal of Neuroscience, volume 24, pages 11457-11462.

(821) Modularity and community structure in networks.   Newman ME.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8577-8582.

(822) Selfish and spiteful behaviour in an evolutionary model.   Hamilton WD.   1970.   Nature, volume 228, pages 1218-1220.

(823) Long-term follow-up of bilateral hypothalamic stimulation for intractable cluster headache.   Leone M, Franzini A, Broggi G, May A and Bussone G.   2004.   Brain, volume 127, pages 2259-2264.

(824) Hypothalamic stimulation in chronic cluster headache: a pilot study of efficacy and mode of action.   Schoenen J, Di Clemente L, Vandenheede M, Fumal A, De Pasqua V, Mouchamps M, Remacle JM and de Noordhout AM.   2006.   Brain, volume 128, pages 940-947.

(825) Precise long-range synchronization of activity and silence in neocortical neurons during slow-wave sleep.   Volgushev M, Chauvette S, Mukovski M and Timofeev I.   2006.   Journal of Neuroscience, volume 26, pages 5665-5672.

(826) Combined application of behavior genetics and microarray analysis to identify regional expression themes and gene-behavior associations. Letwin ME, Kafkafi N, Benjamini Y, Mayo C, Frank BC, Luu T, Lee NH and Elmer GI.   2006.   Journal of Neuroscience, volume 26, pages 5277-5287.

(827) An inhibitor of DNA recombination blocks memory consolidation, but not reconsolidation, in context fear conditioning.   Colon-Cesario M, Wang J, Ramos X, Garcia HG, Davila JJ, Laguna J, Rosado C and Pena de Ortiz S.   2006.   Journal of Neuroscience, volume 26, pages 5524-5533.

(828) Induction of brain region-specific forms of obesity by agouti.   Kas MJ, Tiesjema B, van Dijk G, Garner KM, Barsh GS, Brake OT, Verhaagen J and Adan RA.   2004.   Journal of Neuroscience, volume 24, pages 10176-10181.

(829) Physiological changes in glucose differentially modulate the excitability of hypothalamic melanin-concentrating hormone and orexin neurons in situ.   Burdakov D, Gerasimenko O and Verkhratsky A.   2005.   Journal of Neuroscience, volume 25, pages 2429-2433.

(830) Late-onset leanness in mice with targeted ablation of melanin concentrating hormone neurons.   Alon T and Friedman JM.   2006.   Journal of Neuroscience, volume 26, pages 389-397.

(831) GABAergic mechanisms in regulating the activity state of substantia nigra pars reticulata neurons.   Windels F and Kiyatkin EA.   2006.   Neuroscience, volume 140, pages 1289-1299.

(832) Urocortinergic neurons respond in a differentiated manner to various acute stressors in the Edinger-Westphal nucleus in the rat.   Gaszner B, Csernus V and Kozicz T.   2004.   Journal of Comparative Neurology, volume 480, pages 170-179.

(833) Extending the effects of spike-timing-dependent plasticity to behavioral timescales.   Drew PJ and Abbott LF.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8876-8881.

(834) A metabolic network in the evolutionary context: multiscale structure and modularity.   Spirin V, Gelfand MS, Mironov AA and Mirny LA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 8774-8779.

(835) Interaction between the corticotropin-releasing factor system and hypocretins (orexins): a novel circuit mediating stress response.   Winsky-Sommerer R, Yamanaka A, Diano S, Borok E, Roberts AJ, Sakurai T, Kilduff TS, Horvath TL and de Lecea L.   2004.   Journal of Neuroscience, volume 24, pages 11439-11448.

(836) The subfornical organ is the primary locus of sodium-level sensing by Nax sodium channels for the control of salt-intake behavior.   Hiyama TY, Watanabe E, Okado H and Noda M.   2004.   Journal of Neuroscience, volume 24, pages 9276-9281.

(837) Surround inhibition.   Hallett M.   2003.   Supplements to Clinical Neurophysiology, voume 56, pages 153-159.

(838) Corticotropin-releasing hormone directly activates noradrenergic neurons of the locus ceruleus recorded in vitro.   Jedema HP and Grace AA.   2004.   Journal of Neuroscience, volume 24, pages 9703-9713.

(839) Attentional modulation of perceptual stabilization.   Kanai R and Verstraten FA.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1217-1222.

(840) Are capuchin monkeys (Cebus apella) inequity averse?   Dubreuil D, Gentile MS and Visalberghi E.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1223-1228.

(841) 5-hydroxytryptamine(1a)-like receptor activation in the bed nucleus of the stria terminalis: electrophysiological and behavioral studies.   Levita L, Hammack SE, Mania I, Li XY, Davis M and Rainnie DG.   2004.   Neuroscience, volume 128, pages 583-596.

(842) Serotoninergic axonal contacts on identified cat spinal dorsal horn neurons and their correlation with nucleus raphe magnus stimulation.   Miletic V, Hoffert MJ, Ruda MA, Dubner R and Shigenaga Y.   1984.   Journal of Comparative Neurology, volume 228, pages 129-141.

(843) Construction of genetic oscillators with interlocked feedback networks.   Wang R, Chen L and Aihara K.   2006.   Journal of Theoretical Biology, volume 242, pages 454-463.

(844) Immunohistochemical visualization of corticotropin-releasing factor type 1 (CRF1) receptors in monkey brain.   Kostich WA, Grzanna R, Lu NZ and Largent BL.   2004.   Journal of Comparative Neurology, volume 478, pages 111-125.

(845) Characterization of the neurochemical content of neuronal populations of the lamina terminalis activated by acute hydromineral challenge.   Grob M, Trottier JF, Drolet G and Mouginot D.   2003.   Neuroscience, volume 122, pages 247-257.

(846) Orexin neurons project to diverse sympathetic outflow systems.   Geerling JC, Mettenleiter TC and Loewy AD.   2003.   Neuroscience, volume 122, pages 541-550.

(847) Brain activation during human male ejaculation.   Holstege G, Georgiadis JR, Paans AM, Meiners LC, van der Graaf FH and Reinders AA.   2003.   Journal of Neuroscience, volume 23, pages 9185-9193.

(848) Endogenous glucocorticoids are essential for maintaining prefrontal cortical cognitive function.   Mizoguchi K, Ishige A, Takeda S, Aburada M and Tabira T.   2004.   Journal of Neuroscience, volume 24, pages 5492-5499.

(849) Imaging attentional modulation of pain in the periaqueductal gray in humans.   Tracey I, Ploghaus A, Gati JS, Clare S, Smith S, Menon RS and Matthews PM.   2002.   Journal of Neuroscience, volume 22, pages 2748-2752.

(850) Role of ventrolateral periaqueductal gray neurons in the behavioral and cardiovascular responses to contextual conditioned fear and poststress recovery.   Walker P and Carrive P.   2003.   Neuroscience, volume 116, pages 897-912.

(851) Neuroprotection associated with running: is it a result of increased endogenous neurotrophic factors?   Ang ET, Wong PT, Moochhala S and Ng YK.   2003.   Neuroscience, volume 118, pages 335-345.

(852) Voluntary exercise protects against stress-induced decreases in brain-derived neurotrophic factor protein expression.   Adlard PA and Cotman CW.   2004.   Neuroscience, volume 124, pages 985-992.

(853) Paraventricular nucleus activation of renal sympathetic neurones is synaptically depressed by nitric oxide and glycine acting at a spinal level.   Yang Z, Smith L and Coote JH.   2004.   Neuroscience, volume 124, pages 421-428.

(854) Unfairness, anger and spite: emotional rejections of ultimatum offers.   Pillutla MM and Murnighan JK.   1996.   Organizational Behavior and Human Decision Processes, volume 68, pages 208-224.

(855) Neural basis of irony comprehension in children with autism: the role of prosody and context.   Wang AT, Lee SS, Sigman M and Dapretto M.   2006.   Brain, volume 129, pages 932-943.

(856) Probing the human hippocampus using rCBF: contrasts in schizophrenia.   Medoff DR, Holcomb HH, Lahti AC and Tamminga CA.   2001.   Hippocampus, volume 11, pages 543-550.

(857) Neural basis of aging: the penetration of cognition into action control.   Heuninckx S, Wenderoth N, Debaere F, Peeters R and Swinnen SP.   2005.   Journal of Neuroscience, volume 25, pages 6787-6796.

(858) Neural mechanisms underlying probabilistic category learning in normal aging.   Fera F, Weickert TW, Goldberg TE, Tessitore A, Hariri A, Das S, Lee S, Zoltick B, Meeter M, Myers CE, Gluck MA, Weinberger DR and Mattay VS.   2005.   Journal of Neuroscience, volume 25, pages 11340-11348.

(859) Differential contributions of prefrontal and temporolimbic pathology to mechanisms of psychosis.   Suzuki M, Zhou SY, Takahashi T, Hagino H, Kawasaki Y, Niu L, Matsui M, Seto H and Kurachi M.   2005.   Brain, volume 128, pages 2109-2122.

(860) Time for a shift in focus in schizophrenia: from narrow phenotypes to broad endophenotypes.   Weiser M, van Os J and Davidson M.   2005.   British Journal of Psychiatry, volume 187, pages 203-205.    Comment. Time for a broad phenotype in schizophrenia?   Sanjuan J, Aguilar AJ and de Frutos R.   2006.   British Journal of Psychiatry, volume 188, page 190.

(861) Laterality phenotypes in patients with schizophrenia, their siblings and controls: associations with clinical and cognitive variables.   Dragovic M, Hammond G, Badcock JC and Jablensky A.   2005.   British Journal of Psychiatry, volume 187, pages 221-228.

(862) Altered glucocorticoid immunoregulation in treatment resistant depression.   Bauer ME, Papadopoulos A, Poon L, Perks P, Lightman SL, Checkley S and Shanks N.   2003.   Psychoneuroendocrinology, volume 28, pages 49-65.

(863) Neurocognitive development of the ability to manipulate information in working memory.   Crone EA, Wendelken C, Donohue S, van Leijenhorst L and Bunge SA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 9315-9320.

(864) Regulation of synaptic plasticity in a schizophrenia model.   Gisabella B, Bolshakov VY and Benes FM.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 13301-13306.

(865) Neuroanatomical correlates of behavioural disorders in dementia.   Rosen HJ, Allison SC, Schauer GF, Gorno-Tempini ML, Weiner MW and Miller BL.   2005.   Brain, volume 128, pages 2612-2625.

(866) Regional and laminar differences in in vivo firing patterns of primate cortical neurons.   Shinomoto S, Miyazaki Y, Tamura H and Fuzita I.   2005.   Journal of Neurophysiology, volume 94, pages 567-575.

(867) Three channels of corticothalamic communication during locomotion.   Sirota MG, Swadlow HA and Beloozerova IN.   2005.   Journal of Neuroscience, volume 25, pages 5915-5925.

(868) The sensory cortical representation of the human penis: revisiting somatotopy in the male homunculus.   Kell CA, von Kriegstein K, Rosler A, Kleinschmidt A and Laufs H.   2005.   Journal of Neuroscience, volume 25, pages 5984-5987.

(869) The precuneus: a review of its functional anatomy and behavioural correlates.   Cavanna AE and Trimble MR.   2006.   Brain, volume 129, pages 564-583.

(870) Deciding how to decide: ventromedial frontal lobe damage affects information acquisition in multi-attribute decision making.   Fellows LK.   2006.   Brain, volume 129, pages 944-952.

(871) Laminar and columnar organization of ascending excitatory projections to layer 2/3 pyramidal neurons in rat barrel cortex.   Shepherd GM and Svoboda K.   2005.   Journal of Neuroscience, volume 25, pages 5670-5679.

(872) Theta oscillations in human cortex during a working memory task: evidence for local generators.   Raghavachari S Lisman JE, Tully M, Madsen JR, Bromfield E and Kahana MJ.   2006.   Journal of Neurophysiology, volume 95, pages 1630-1638.

(873) Anatomical abnormalities in dopaminoceptive regions of the cerebral cortex of dopamine D(1) receptor mutant mice.   Stanwood GD, Parlaman JP and Levitt P.   2005.   Journal of Comparative Neurology, volume 487, pages 270-282.

(874) Triple dissociation in the medial temporal lobes: recollection, familiarity and novelty.   Daselaar SM, Fleck MS and Cabeza RE.   2006.   Journal of Neurophysiology, volume 96, pages 1902-1911.

(875) Perspective: maternal kin groups and the origins of asymmetric genetic systems-genomic imprinting, haplodiploidy, and parthenogenesis.   Normark BB.   2006.   Evolution. International Journal of Organic Evolution, volume 60, pages 631-642.   See "more 'abstemious' expression of maternally derived alleles and more 'greedy' expression of paternally derived alleles.".

(876) Operculoinsular cortex encodes pain intensity at the earliest stages of cortical processing as indicated by amplitude of laser-evoked potentials in humans.   Iannetti GD, Zambreanu L, Cruccu G and Tracey I.   2005.   Neuroscience, volume 131, pages 199-208.

(877) Intrinsic connections of the cingulate cortex in the rat suggests the existence of multiple functionally segregated networks.   Jones BF, Groenewegen HJ and Witter MP.   2005.   Neuroscience, volume 133, pages 193-207.

(878) A subpopulation of neurons in the medial prefrontal cortex encodes emotional learning with burst and frequency codes through a dopamine D4 receptor-dependent basolateral amygdala input.   Laviolette SR, Lipski WJ and Grace AA.   2005.   Journal of Neuroscience, volume 25, pages 6066-6075.

(879) Psychiatric symptoms and parietal disease: differential diagnosis.   Critchley M.   1964.   Proceedings of the Royal Society of Medicine, volume 57, pages 422-428.

(880) Awareness of the functioning of one's own limbs mediated by the insular cortex?   Karnath HO, Baier B and Nagele T.   2005.   Journal of Neuroscience, volume 25, pages 7134-7138.

(881) Firing characteristics of deep layer neurons in prefrontal cortex in rats performing spatial working memory tasks.   Jung MW, Qin Y, McNaughton BL and Barnes CA.   1998.   Cerebral Cortex, volume 8, pages 437-450.

(882) Selectivity for the human body in the fusiform gyrus.   Peelen MV and Downing PE.   2005.   Journal of Neurophysiology, volume 93, pages 603-608.

(883) Separate face and body selectivity on the fusiform gyrus.   Schwarzlose RF, Baker CI and Kanwisher N.   2005.   Journal of Neuroscience, volume 25, pages 11055-11059.

(884) Medial prefrontal cortex cells show dynamic modulation with the hippocampal theta rhythm dependent on behavior.   Hyman JM, Zilli EA, Paley AM and Hasselmo ME.   2005.   Hippocampus, volume 15, pages 739-749.

(885) Neural mechanism in anterior prefrontal cortex for inhibition of prolonged set interference.   Konishi S, Chikazoe J, Jimura K, Asari T and Miyashita Y.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 12584-12588.

(886) Cortical processing of visceral and somatic stimulation: differentiating pain intensity from unpleasantness.   Dunckley P, Wise RG, Aziz Q, Painter D, Brooks J, Tracey I and Chang L.   2005.   Neuroscience, volume 133, pages 533-542.

(887) Neuromodulation of spike-timing precision in sensory neurons.   Billimoria CP, DiCaprio RA, Birmingham JT, Abbott LF and Marder E.   2006.   Journal of Neuroscience, volume 26, pages 5910-5919.

(888) Noradrenaline unmasks novel self-reinforcing motor circuits within the mammalian spinal cord.   Machacek DW and Hochman S.   2006.   Journal of Neuroscience, volume 26, pages 5920-5928.

(889) Role of the olivo-cerebellar system in timing.   Xu D, Liu T, Ashe J and Bushara KO.   2006.   Journal of Neuroscience, volume 26, pages 5990-5995.

(890) Ipsilateral input modifies the primary somatosensory cortex response to contralateral skin flutter.   Tommerdahl M, Simons SB, Chiu JS, Favorov O and Whitsel BL.   2006.   Journal of Neuroscience, volume 26, pages 5970-5977.

(891) Role of substantia nigra-amygdala connections in surprise-induced enhancement of attention.   Lee HJ, Youn JM, O MJ, Gallagher M and Holland PC.      2006.   Journal of Neuroscience, volume 26, pages 6077-6081.

(892) Prefrontal set activity predicts rule-specific neural processing during subsequent cognitive performance.   Sakai K and Passingham RE.   2006.   Journal of Neuroscience, volume 26, pages 1211-1218.

(893) The involvement of the orbitofrontal cortex in the experience of regret.   Camille N, Coricelli G, Sallet J, Pradat-Diehl P, Duhamel JR and Sirigu A.   2004.   Science, volume 304, pages 1167-1170.

(894) The functional neuroanatomy of classic delayed response tasks in humans and the limitations of cross-method convergence in prefrontal function.   Turner GR and Levine B.   2006.   Neuroscience, volume 139, pages 327-337.

(895) Visual and nonvisual contributions to three-dimensional heading selectivity in the medial superioral temporal area.   Gu Y, Watkins PV, Angelaki DE and DeAngelis GC.   2006.   Journal of Neuroscience, volume 26, pages 73-85.

(896) Fear conditioning following unilateral temporal lobectomy: dissociation of conditioned startle potentiation and autonomic learning.   Weike AI, Hamm AO, Schupp HT, Runge U, Schroeder RW and Kessler C.   2005.   Journal of Neuroscience, volume 25, pages 11117-11124.

(897) Specialization in the medial temporal lobe for processing of objects and scenes.   Lee AC, Buckley MJ, Pegman SJ, Spiers H, Scahill VL, Gaffan D, Bussey TJ, Davies RR, Kapur N, Hodges JR and Graham KS.   2005.   Hippocampus, volume 15, pages 782-797.   The concept "...object viewpoint independent perception..." is elliptical to the point of incomprehensibility.

(898) Pain and the body schema: evidence for peripheral effects on mental representations of movement.   Schwoebel J, Friedman R, Duda N and Coslett HB.   2001.   Brain, volume 124, pages 2098-2104.

(899) Neurons in the rostral cingulate motor area monitor multiple phases of visuomotor behavior with modest parametric selectvity.   Hoshi E, Sawamura H and Tanji J.   2005.   Journal of Neurophysiology, volume 94 pages 640-656.

(900) Context-dependent stimulation effects on saccade initiation in the presupplementary motor area of the monkey.   Isoda M.   2005.   Journal of Neurophysiology, volume 93, pages 3016-3022.

(901) Prolactin-releasing peptide is a potent mediator of stress responses in the brain through the hypothalamic paraventricular nucleus.   Mera T, Fujihara H, Kawasaki M, Hashimoto H, Saito T, Shibata M, Saito J, Oka T, Tsuji S, Onaka T and Ueta Y.   2006.   Neuroscience, volume 141, pages 1069-1086.

(902) Mice expressing constitutively active G(s)alpha exhibit stimulus encoding deficits similar to those observed in schizophrenia patients.   Maxwell CR, Liang Y, Kelly MP, Kanes SJ, Abel T and Siegel SJ.   2006.   Neuroscience, volume 141, pages 1257-1264.

(903) A spatially structured network of inhibitory and excitatory connections directs impulse traffic within the lateral amygdala.   Samson RD and Pare D.   2006.   Neuroscience, volume 141, pages 1599-1609.

(904) Neural correlates of priming on occluded figure interpretation in human fusiform cortex.   Liu LC, Plomp G, van Leeuwen C and Ioannides AA.   2006.   Neuroscience, volume 141, pages 1585-1597.

(905) Endocannabinoid signaling in rat somatosensory cortex: laminar differences and involvement of specific interneuron types.   Bodor AL, Katona I, Nyiri G, Mackie K, Ledent C, Hajos N and Freund TF.   2005.   Journal of Neuroscience, volume 25, pages 6845-6856.

(906) Declarative memory consolidation in humans: a prospective functional magnetic resonance imaging study.   Takashima A, Petersson KM, Rutters F, Tendolkar I, Jensen O, Zwarts MJ, McNaughton BL and Fernandez G.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 756-761.

(907) Cytoarchitectonic subdivisions of the dorsolateral frontal cortex of the marmoset monkey (Callithrix jacchus), and their projections to dorsal visual areas.   Burman KJ, Palmer SM, Gamberini M and Rosa MG.   2006.   Journal of Comparative Neurology, volume 495, pages 149-172.

(908) Parietal cortex mediates voluntary control of spatial and nonspatial auditory attention.   Shomstein S and Yantis S.   2006.   Journal of Neuroscience, volume 26, pages 435-439.

(909) Working memory for order information: multiple cognitive and neural mechanisms.   Marshuetz C and Smith EE.   2006.   Neuroscience, volume 139, pages 311-316.   Presumably the second sentence of the abstract should describe general supervisory processes, and also processes that maintain fine-grained temporal position information.

(910) Effects of unilateral prefrontal lesions on familiarity, recollection, and source memory.   Duarte A, Ranganath C and Knight RT.   2005.   Journal of Neuroscience, volume 25, pages 8333-8337.

(911) Delay-period activity in visual, visuomovement, and movement neurons in the frontal eye field.   Lawrence BM, White RL and Snyder LH.   2005.   Journal of Neurophysiology, volume 94, pages 1498-1508.

(912) Fluent conceptual processing and explicit memory for faces are electrophysiologically distinct.   Voss JL and Paller KA.   2006.   Journal of Neuroscience, volume 26, pages 926-933.

(913) Prefrontal control of the amygdala.   Likhtik E, Pelletier JG, Paz R and Pare D.   2005.   Journal of Neuroscience, volume 25, pages 7429-7437.

(914) Predicting short-term stock fluctuations by using processing fluency.   Alter AL and Oppenheimer DM.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 9369-9372.

(915) microRNAs exhibit high frequency genomic alterations in human cancer.   Zhang L, Huang J, Yang N, Greshock J, Megraw MS, Giannakakis A, Liang S, Naylor TL, Barchetti A, Ward MR, Yao G, Medina A, O'brien-Jenkins A, Katsaros D, Hatzigeorgiou A, Gimotty PA, Weber BL and Coukos G.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 9136-9141.

(916) Ipsilateral cortical connections of motor, premotor, frontal eye, and posterior parietal fields in a prosimian primate, Otolemur garnetti.   Fang PC, Stepniewska I and Kaas JH.   2005.   Journal of Comparative Neurology, volume 490, pages 305-333.

(917) Rapid developmental switch in the mechanisms driving early cortical columnar networks.   Dupont E, Hanganu IL, Kilb W, Hirsch S and Luhmann HJ.   2006.   Nature, volume 439, pages 79-83.

(918) Comparison of the effects of bilateral orbital prefrontal cortex lesions and amygdala lesions on emotional responses in rhesus monkeys.   Izquierdo A, Suda RK and Murray EA.   2005.   Journal of Neuroscience, volume 25, pages 8534-8542.

(919) Morphological correlates of corticosteroid-induced changes in prefrontal cortex-dependent behaviors.   Cerqueira JJ, Pego JM, Taipa R, Bessa JM, Almeida OF and Sousa N.   2005.   Journal of Neuroscience, volume 25, pages 7792-7800.

(920) Comparison of anterior cingulate and primate somatosensory neuronal responses to noxious laser-heat stimuli in conscious, behaving rats.   Kuo CC and Yen CT.   2005.   Journal of Neurophysiology, volume 94, pages 1825-1836.

(921) Delayed onset and resolution of pain: some observations and implications.   Schott GD.   2001.   Brain, volume 124, pages 1067-1076.

(922) Contributions of anterior cingulate cortex to behaviour.   Devinsky O, Morrell MJ and Vogt BA.   1995.   Brain, volume 118, pages 279-306.

(923) Material-specific lateralization in the medial temporal lobe and prefrontal cortex during memory encoding.   Golby AJ, Poldrack RA, Brewer JB, Spencer D, Desmond JE, Aron AP and Gabrieli JD.   2001.   Brain, volume 124, pages 1841-1854.

(924) Does gender play a role in functional asymmetry of ventromedial prefrontal cortex?   Tranel D, Damasio H, Denburg NL and Bechara A.   2005.   Brain, volume 128, pages 2872-2881.   It is tendentious to enable general comments about the genders, on the basis of eight patients, configured as two male pairs, one female pair and two female individuals. Potential sampling error should have been acknowledged in the abstract.

(925) The role of ventral frontostriatal circuitry in reward-based learning in humans.   Galvan A, Hare TA, Davidson M, Spicer J, Glover G and Casey BJ.   2005.   Journal of Neuroscience, volume 25, pages 8650-8656.

(926) Prefrontal cortex in the rat: projections to subcortical autonomic, motor, and limbic centers.   Gabbott PL, Warner TA, Jays PR, Salway P and Busby SJ.   2005.   Journal of Comparative Neurology, volume 492, pages 145-177.

(927) Lateral somatotopic organization during imagined and prepared movements.   Michelon P, Vettel JM and Zacks JM.   2006.   Journal of Neurophysiology, volume 95, pages 811-822.

(928) Evidence for hierarchical error processing in the human brain.   Krigolson OE and Holroyd CB.   2006.   Neuroscience, volume 137, pages 13-17.   How can temporally distinct brain potentials suggest an interaction, as distinct from a lack of interaction? What degree of temporal distinctness would have been required for the experimenters to have relinquished their preconceived idea of an hierarchically organised system?

(929) Feedback and feedforward control of frequency tuning to naturalistic stimuli.   Chacron MJ, Maler L and Bastian J.   2005.   Journal of Neuroscience, volume 25, pages 5521-5532.

(930) Emerging patterns of neuronal responses in supplementary and primary motor areas during sensorimotor adaptation.   Paz R, Natan C, Boraud T, Bergman H and Vaadia E.   2005.   Journal of Neuroscience, volume 25, pages 10941-10951.

(931) Stable ensemble performance with single-neuron variability during reaching movements in primates.   Carmena JM, Lebedev MA, Henriquez CS and Nicolelis MA.   2005.   Journal of Neuroscience, volume 25, pages 10712-10716.

(932) Chronometry of visual responses in frontal eye field, supplementary eye field and anterior cingulate cortex.   Poujet P, Emeric EE, Stuphorn V, Reis KM and Schall JD.   2005.   Journal of Neurophysiology, volume 94, pages 2086-2092.

(933) Influence of predator stress on the consolidation versus retrieval of long-term spatial memory and hippocampal spinogenesis.   Diamond DM, Campbell AM, Park CR, Woodson JC, Conrad CD, Bachstetter AD and Mervis RF.   2006.   Hippocampus, volume 16, pages 571-576.

(934) Independent controls of attentional influences in primary and secondary somatosensory cortex.   Chapman CE and Meftah EM.   2005.   Journal of Neurophysiology, volume 94, pages 4094-4107.

(935) Input-output organization of jaw movement-related areas in monkey frontal cortex.   Hatanaka N, Tokuno H, Nambu A, Inoue T and Takada M.   2005.   Journal of Comparative Neurology, volume 492, pages 401-425.

(936) Cholinergic inhibition of neocortical pyramidal neurons.   Gulledge AT and Stuart GJ.   2005.   Journal of Neuroscience, volume 25, pages 10308-10320.

(937) The future of cognitive-behavioural therapy for psychosis: not a quasi-neuroleptic.   Birchwood M and Trower P.   2006.   British Journal of Psychiatry, volume 188, pages 107-108.

(938) Gene expression deficits in a subclass of GABA neurons in the prefrontal cortex of subjects with schizophrenia.   Hashimoto T, Volk DW, Eggan SM, Mirnics K, Pierri JN, Sun Z, Sampson AR and Lewis DA.   2003.   Journal of Neuroscience, volume 23, pages 6315-6326.

(939) Dopamine modulation of perisomatic and peridendritic inhibition in prefrontal cortex.   Gao W-J, Wang Y, and Goldman-Rakic PS.   2003.   Journal of Neuroscience, volume 23, pages 1622-1630.   The reference to both pyramidal neurones and pyramidal cells does not appear to have any anatomical basis, and confuses, because the interneurone that is described as contacting the neurone actually contacts the soma, and the interneurone that is described as contacting the cell actually contacts the dendrites.

(940) DISC1 immunoreactivity at the light and ultrastructural level in the human neocortex.   Kirkpatrick B, Xu L, Cascella N, Ozeki Y, Sawa A and Roberts RC.   2006.   Journal of Comparative Neurology, volume 497, pages 436-450.

(941) Opposing roles of D1 and D2 receptors in appetitive conditioning.   Eyny YS and Horvitz JC.   2003.   Journal of Neuroscience, volume 23, pages 1584-1587.

(942) Catechol-O-methyltransferase genotype and dopamine regulation in the human brain.   Akil M, Kolachana BS, Rothmond DA, Hyde TM, Weinberger DR and Kleinman JE.   2003.   Journal of Neuroscience, volume 23, pages 2008-2013.

(943) Dopamine release in response to a psychological stress in humans and its relationship to early life maternal care: a positron emission tomography study using [11C]raclopride.   Prussner JC, Champagne F, Meaney MJ and Dagher A.   2004.   Journal of Neuroscience volume 24, pages 2825-2831.

(944) Enhancement of working memory in aged monkeys by a sensitizing regimen of dopamine D1 receptor stimulation.   Castner SA and Goldman-Rakic PS.   2004.   Journal of Neuroscience, volume 24, pages 1446-1450.

(945) The columnar organization of the neocortex.   Mountcastle VB.   1997.   Brain, volume 120, pages 701-722.

(946) Origins of cortical interneuron subtypes.   Xu Q, Cobos I, De La Cruz E, Rubenstein JL and Anderson SA.   2004.   Journal of Neuroscience, volume 24, pages 2612-2622.

(947) Circadian rhythm generation and entrainment in astrocytes.   Prolo LM, Takahashi JS and Herzog ED.   2005.   Journal of Neuroscience, volume 25, pages 404-408.

(948) Frequency-dependent survival in natural guppy populations.   Olendorf R, Rodd FH, Punzalan D, Houde AE, Hurt C, Reznick DN and Hughes KA.   2006.   Nature, volume 441, pages 633-636.

(949) Prefrontal activity during serial probe reproduction task: encoding, mnemonic and retrieval processes.   Inoue M and Mikami A.   2006.   Journal of Neurophysiology, volume 95, pages 1008-1041.   How can C2 be both an object and a period? Does the C in CT refer to an object, or to a period during which that object was presented? This abstract is a test of working memory, rather than an explication of it.

(950) Cerebellar damage produces selective deficits in verbal working memory.   Ravizza SM, McCormick CA, Schlerf JE, Justus T, Ivry RB and Fiez JA.   2006.   Brain, volume 129, pages 306-320.    Comment. Thinking about the cerebellum.   Glickstein M.   2006.   Brain, volume 129, pages 288-290.    Comment. Cognition, emotion and the cerebellum.   Schmahmann JD and Caplan D.   2006.   Brain, volume 129, pages 290-292.

(951) Functional circuitry underlying visual neglect.   Rushmore RJ, Valero-Cabre A, Lomber SG, Hilgetag CC and Payne BR.   2006.   Brain, volume 129, pages 1803-1821.

(952) Fitness cost of LINE-1 (L1) activity in humans.   Boissinot S, Davis J, Entezam A, Petrov D and Furano AV.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 9590-9594.

(953) Synaptic interactions of late-spiking neocortical neurons in layer 1.   Chu Z, Galarreta M and Hestrin S.   2003.   Journal of Neuroscience, volume 23, pages 96-102.

(954) Neuroglial metabolism in the awake rat brain: CO2 fixation increases with brain activity.   Oz G, Berkich DA, Henry PG, Xu Y, LaNoue K, Hutson SM and Gruetter R.   2004.   Journal of Neuroscience, volume 24, pages 11273-11279.

(955) Stress and adult neurogenesis.   Mirescu C and Gould E.   2006.   Hippocampus, volume 16, pages 233-238.

(956) Prefrontal cortex stimulation induces 2-arachidonoyl-glycerol-mediated suppression of excitation in dopamine neurons.   Melis M, Perra S, Muntoni AL, Pillolla G, Lutz B, Marsicano G, DiMarzo V, Gessa GL and Pistis M.   2004.   Journal of Neuroscience, volume 24, pages 10707-10715.

(957) Evidence for a selective prefrontal cortical gaba(b) receptor-mediated inhibition of glutamate release in the ventral tegmental area: a dual probe microdialysis study in the awake rat.   Harte M and O'Connor WT.   2005.   Neuroscience, volume 130, pages 215-222.

(958) Ectopic action potential generation in cortical interneurons during synchronized GABA responses.   2005.   Keros S and Hablitz JJ.   Journal of Neuroscience, volume 131, pages 833-842.

(959) Frontoparietal control of spatial attention and motor intention in human EEG.   Praamstra P, Boutsen L and Humphreys GW.   2005.   Journal of Neurophysiology, volume 94, pages 764-774.

(960) Control of attention shifts between vision and audition in human cortex.   Shomstein S and Yantis S.   2004.   Journal of Neuroscience, volume 24, pages 10702-10706.

(961) The neural mechanisms for minimizing cross-modal distraction.   Weissman DH, Warner LM and Woldorff MG.   2004.   Journal of Neuroscience, volume 24, pages 10941-10949.

(962) Localizing P300 generators in visual target and distractor processing: a combined event-related potential and functional magnetic resonance imaging study.   Bledowski C, Prvulovic D, Hoechstetter K, Scherg M, Wibral M, Goebel R and Linden DE.   2004.   Journal of Neuroscience, volume 24, pages 9353-9360.

(963) Brain volume in first-episode schizophrenia: systematic review and meta-analysis of magnetic resonance imaging studies.   Steen RG, Mull C, McClure R, Hamer RM and Lieberman JA.   2006.   British Journal of Psychiatry, volume 188, pages 510-518.

(964) Functional organization of human intraparietal and frontal cortex for attending, looking, and pointing.   Astafiev SV, Shulman GL, Stanley CM, Snyder AZ, Van Essen DC and Corbetta M.   2003.   Journal of Neuroscience, volume 23, pages 4689-4699.

(965) Human eye fields in the frontal lobe as studied by epicortical recording of movement-related cortical potentials.   Yamamoto J, Ikeda A, Satow T, Matsuhashi M, Baba K, Yamane F, Miyamoto S, Mihara T, Hori T, Taki W, Hashimoto N and Shibasaki H.   2004.   Brain, volume 127, pages 873-887.

(966) A rapid and precise on-response in posterior parietal cortex.   Bisley JW, Khrishna BS and Goldberg ME.   2004.   Journal of Neuroscience, volume 24, pages 1833-1838.

(967) "What" becoming "where": functional magnetic resonance imaging evidence for pragmatic relevance driving premotor cortex.   Wolfensteller U, Schubotz RI and von Cramon DY.   2004.   Journal of Neuroscience, volume 24, pages 10431-10439.

(968) How self-initiated memorized movements become automatic: a functional MRI study.   Wu T, Kansaku K and Hallett M.   2004.   Journal of Neurophysiology, volume 91, pages 1690-1698.

(969) Functional properties of fast spiking interneurons and their synaptic connections with pyramidal cells in primate dorsolateral prefrontal cortex.   Gonzalez-Burgos G, Krimer LS, Povysheva NV, Barrionuevo G and Lewis DA.   2005.   Journal of Neurophysiology, volume 93, pages 942-953.

(970) Unconscious vision: new insights into the neuronal correlate of blindsight using diffusion tractography.   Leh SE, Johansen-Berg H and Ptito A.   2006.   Brain, volume 129, pages 1822-1832.

(971) New insights into the anatomo-functional connectivity of the semantic system: a study using cortico-subcortical electrostimulations.   Duffau H, Gatignol P, Mandonnet E, Peruzzi P, Tzourio-Mazoyer N and Capelle L.   2005.   Brain, volume 128, pages 797-810.

(972) Finger and face representations in the ipsilateral precentral motor areas in humans.   Hanakawa T, Parikh S, Bruno MK and Hallett M.   2005.   Journal of Neurophysiology, volume 93, pages 2950-2958.

(973) The dominance hierarchy and the evolution of mental illness.   Price JS.   1967.   The Lancet, volume 2, pages 243-246.

(974) The influence of social hierarchy on primate health.   Sapolsky RM.   2005.   Science, volume 308, pages 648-652.

(975) Functional consequences of presynaptic inhibition during behaviorally-relevant activity.   Frerking M and Ohliger-Frerking PA.   2006.   Journal of Neurophysiology, volume 96, pages 2139-2143.

(976) Differential controls over tactile detection in humans by motor commands and peripheral reafference.   Chapman CE and Beauchamp E.   2006.   Journal of Neurophysiology, volume 96, pages 1664-1675.

(977) Differential involvement of parietal and precentral regions in movement preparation and motor intention.   Thoenissen D, Zilles K and Toni L.   2002.   Journal of Neuroscience, volume 22, pages 9024-9034.

(978) Spatial attention and memory versus motor preparation: premotor cortex involvement as revealed by fMRI.   Simon SR, Meunier M, Piettre L Berardi AM, Segebarth CM and Boussaoud D.   2002.   Journal of Neurophysiology, volume 88, pages 2047-2057.

(979) Sensorimotor integration in the precentral gyrus: polysensory neurons and defensive movements.   Cooke DF and Graziano MSA.   2004.   Journal of Neurophysiology, volume 91, pages 1648-1660.

(980) Attention and stimulus characteristics determine the locus of motor-sequence encoding. A PET study.   Hazeltine E, Grafton ST and Ivry R.   1997.   Brain, volume 120, pages 123-140.

(981) Believe in your placebo.   Seminowicz DA.   2006.   Journal of Neuroscience, volume 26, pages 4453-4454.

(982) Spite and altruism in gulls.   Pierotti R.   1980.   The American Naturalist, volume 115, pages 290-300.

(983) Bright light treatment of winter depression.   Eastman CI, Young MA, Fogg LF, Liu L and Meaden PM.   1988.   Archives of General Psychiatry, volume 55, pages 883-889.

(984) Computational and neurobiological mechanisms underlying cognitive flexibility.   2006.   Badre D and Wagner AD.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 7186-7191.

(985) Synergy and discounting of cooperation in social dilemmas.   Hauert C, Michor F, Nowak MA and Doebeli M.   2006.   Journal of Theoretical Biology, volume 239, pages 195-202.

(986) State-dependent gating of sensory inputs by zona incerta.   Trageser JC, Burke KA, Masri R, Li Y, Sellers L and Keller A.   2006.   Journal of Neurophysiology, volume 96, pages 1456-1493.

(987) The sleep slow oscillation as a traveling wave.   Massimini M, Huber R, Ferrarelli F , Hill S and Tononi G.   2004.   Journal of Neuroscience, volume 24, pages 6862-6870.

(988) Hippocampal slow oscillation: a novel EEG state and its coordination with ongoing neocortical activity.   Wolansky T, Clement EA, Peters SR, Palczak MA and Dickson CT.   2006.   Journal of Neuroscience, volume 26, pages 6213-6229.

(989) The neural basis of imitation is body part specific.   Goldenberg G and Karnath HO.   2006.   Journal of Neuroscience, volume 26, pages 6282-6287.

(990) Temporal and spatial dynamics of brain structure changes during extensive learning.   Draganski B, Gaser C, Kempermann G, Kuhn HG, Winkler J, Buchel C and May A.   2006.   Journal of Neuroscience, volume 26, pages 6314-6317.

(991) Changes in functional connectivity within the rat striatopallidal axis during global brain activation in vivo.   Magill PJ, Pogosyan A, Sharott A, Csicsvari J, Bolam JP and Brown P.   2006.   Journal of Neuroscience, volume 26, pages 6318-6329.

(992) The statistical computation underlying contrast gain control.   Bonin V, Mante V and Carandini M.   2006.   Journal of Neuroscience, volume 26, pages 6346-6353.

(993) Neurobiological substrates of dread.   Berns GS, Chappelow J, Cekic M, Zink CF, Pagnoni G and Martin-Skurski ME.   2006.   Science, volume 312, pages 754-758.

(994) Medial versus lateral frontal lobe contributions to voluntary saccade control as revealed by the study of patients with frontal lobe degeneration.   Boxer AL, Garbutt S, Rankin KP, Hellmuth J, Neuhaus J, Miller BL and Lisberger SG.   2006.   Journal of Neuroscience, volume 26, pages 6354-6363.

(995) Striatal functional alteration in adolescents characterized by early childhood behavioral inhibition.   Guyer AE, Nelson EE, Perez-Edgar K, Hardin MG, Roberson-Nay R, Monk CS, Bjork JM, Henderson HA, Pine DS, Fox NA and Ernst M.   2006.   Journal of Neuroscience, volume 26, pages 6399-6405.

(996) The mellow years?: neural basis of improving emotional stability over age.   Williams LM, Brown KJ, Palmer D, Liddell BJ, Kemp AH, Olivieri G, Peduto A and Gordon E.   2006.   Journal of Neuroscience, volume 26, pages 6422-6430.

(997) Origins of GABA(A) and GABA(B) receptor-mediated responses of globus pallidus induced after stimulation of the putamen in the monkey.   Kita H, Chiken S, Tachibana Y and Nambu A.   2006.   Journal of Neuroscience, volume 26, pages 6554-6562.

(998) Subventricular zone-derived neuroblasts migrate and differentiate into mature neurons in the post-stroke adult striatum.   Yamashita T, Ninomiya M, Hernandez Acosta P, Garcia-Verdugo JM, Sunabori T, Sakaguchi M, Adachi K, Kojima T, Hirota Y, Kawase T, Araki N, Abe K, Okano H and Sawamoto K.   2006.  Journal of Neuroscience, volume 26, pages 6627-6636.

(999) The circadian basis of winter depression.   Lewy AJ, Lefler BJ, Emens JS and Bauer VK.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 7414-7419.

(1000) Cooperation experiments: coordination through communications versus acting apart together.   Noë R.   2006.   Animal Behaviour, volume 71, pages 1-18.

(1001) Conjunctive representation of position, direction, and velocity in entorhinal cortex.   Sargolini F, Fyhn M, Hafting T, McNaughton BL, Witter MP, Moser M-B and Moser EI.   2006.   Science, volume 312, pages 758-762.    Comment. The map in the brain: grid cells may help us navigate.   Heyman K.   2006.   Science, volume 312, pages 680-681.

(1002) Hypothalamic mTOR signaling regulates food intake.   Cota D, Proulx K, Blake Smith KA, Kozma SC, Thomas G, Woods SC and Seeley RJ.   2006.   Science, volume 312, pages 927-930.    Comment. Regulating energy balance: the substrate strikes back.   Flier JS.   2006.   Science, volume 312, pages 861-864.

(1003) A DNA insulator prevents repression of a targeted X-linked transgene but not its random or imprinted X inactivation.   Ciavatta D, Kalantry S, Magnuson T and Smithies O.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 9958-9963.

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(1008) Image scoring and cooperation in a cleaner fish mutualism.   Bshary R and Grutter AS.   2006.   Nature, volume 441, pages 975-978.

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(1010) Mammalian cochlear supporting cells can divide and trans-differentiate into hair cells.   White PM, Doetzlhofer A, Lee YS, Groves AK and Segil N.   2006.   Nature, volume 441, pages 984-987.

(1011) Rapid-actin based plasticity in dendritic spines.   Fischer M, Kaech S, Knutti D and Matus A.   1998.   Neuron, volume 20, pages 847-854.    Comment. Dancing dendrites.   Edwards FA.   1998.   Nature, volume 194, pages 129-130.

(1012) Dendritic spine changes associated with hippocampal long-term synaptic plasticity.   Engert F and Bonhoeffer T.   1999.   Nature, volume 399, pages 66-70.    Comment. A spine to remember.   Andersen P.   1999.   Nature, volume 399, pages 19-21.

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(1014) Experience-dependent and cell-type specific spine growth in the neocortex.   Holtmaat A, Wilbrecht L, Knott GW, Welker E and Svoboda K.   2006.   Nature, volume 441, pages 979-983.

(1015) Internally stimulated movement sensations during motor imagery activate cortical motor areas and the cerebellum.   Naito E, Kochiyama, Kitada R, Nakamura S, Matsumura M, Yonekura Y and Sadato N.   2002.   Journal of Neuroscience, volume 22, pages 3683-3691.

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(1017) Earlier development of the accumbens relative to orbitofrontal cortex might underlie risk-taking behavior in adolescents.   Galvan A, Hare TA, Parra CE, Penn J, Voss H, Glover G and Casey BJ.   2006.   Journal of Neuroscience, volume 26, pages 6885-6892.

(1018) Lesions of the amygdala that spare adjacent cortical regions do not impair memory or exacerbate the impairment following lesions of the hippocampal formation.   Zola-Morgan S, Squire LR and Amaral DG.   1989.   Journal of Neuroscience, volume 9, pages 1922-1936.

(1019) The impact of early and late damage to the human amygdala on "theory of mind" reasoning.   Shaw P, Lawrence EJ, Radbourne C, Bramham J, Polkey CE and David AS.   2004.   Brain, volume 127, pages 1535-1548.

(1020) The impact of extensive medial frontal lobe damage on "Theory of Mind" and cognition.   Bird CM, Castelli F, Malik O, Frith U and Husain M.   2004.   Brain, volume 127, pages 914-928.

(1021) Intra-operative mapping of cortical areas involved in reading in mono- and bilingual patients.   Roux FE, Lubrano V, Lauwers-Cances V, Tremoulet M, Mascott CR and Demonet JF.   2004.   Brain, volume 127, pages 1796-1810.

(1022) Behavioural uniformity as a response to cues of predation risk.   Szulkin M, Dawidowicz P and Dodson SI.   2006.   Animal Behaviour, volume 71, pages 1013-1019.

(1023) Rhesus monkeys, Macaca mulatta, know what others can and cannot hear.   Santos LR, Nissen AG and Ferrugia JA.   2006.   Animal Behaviour, volume 71, pages 1175-1181.

(1024) Sheep self-medicate when challenged with illness-inducing foods.   Villalba JJ, Provenza FD and Shaw R.   2006.   Animal Behaviour, volume 71, pages 1131-1139.

(1025) Neuronal activity in primate orbitofrontal cortex reflects the value of time.   Roesch MR and Olson CR.   2005.   Journal of Neurophysiology, volume 94, pages 2457-2471.

(1026) Is fearfulness a trait that can be measured with behavioural tests? A validation of four fear tests for Japanese quail.   Miller KA, Garner JP and Mench JA.   2006.   Animal Behaviour, volume 71, pages 1323-1334.

(1027) The effect of handling time on temporal discounting in two New World primates.   Rosati AG, Stevens JR and Hauser MD.   2006.   Animal Behaviour, volume 71, pages 1379-1387.

(1028) Personality predicts brain responses to cognitive demands.   Kumari V, ffytche DH, Williams SC and Gray JA.   2004.   Journal of Neuroscience, volume 24, pages 10636-10641.

(1029) Autonomic asymmetry in migraine: augmented parasympathetic activation in left unilateral migraineurs.   Avnon Y, Nitzan M, Sprecher E, Rogowski Z and Yarnitsky D.   2004.   Brain, volume 127, pages 2099-2108.

(1030) Cortical GABA interneurons in neurovascular coupling: relays for subcortical vasoactive pathways.   Cauli B, Tong XK, Rancillac A, Serluca N, Lambolez B, Rossier J and Hamel E.   2004.   Journal of Neuroscience, volume 24, pages 8940-8949.

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(1034) Lateralized changes in autonomic arousal during emotional processing in patients with unilateral temporal lobe seizure onset.   Lee GP, Meador KJ, Loring DW and Bradley KP.   2002.   International Journal of Neuroscience, volume 112, pages 743-757.

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(1042) Lack of habituation causes high intensity dependence of auditory evoked cortical potentials in migraine.   Ambrosini A, Rossi P, De Pasqua V, Pierelli F and Schoenen J.   2003.   Brain, volume 126, pages 2009-2015.

(1043) Somatosensory evoked high-frequency oscillations reflecting thalamo-cortical activity are decreased in migraine patients between attacks.   Coppola G, Vandenheede M, Di Clemente L, Ambrosini A, Fumal A, De Pasqua V and Schoenen J.   2005.   Brain, volume 128, pages 98-103.

(1044) Propranolol modulates trigeminovascular responses in thalamic ventroposteromedial nucleus: a role in migraine?    Shields KG and Goadsby PJ.   2005.   Brain, volume 128, pages 86-97.

(1045) Central neuromodulation in chronic migraine patients with suboccipital stimulators: a PET study.   Matharu MS, Bartsch T, Ward N, Frackowiak RS, Weiner R and Goadsby PJ.   2004.   Brain, volume 127, pages 220-230.

(1046) Working memory and long-term memory for faces: evidence from fMRI and global amnesia for involvement of the medial temporal lobes.   Nichols EA, Kao YC, Verfaellie M and Gabrieli JD.   2006.   Hippocampus, volume 16, pages 604-616.

(1047) Functional specialization within medial frontal cortex of the anterior cingulate for evaluating effort-related decisions.   Walton ME, Bannerman DM, Alterescu K and Rushworth MF.   2003.   Journal of Neuroscience, volume 23, pages 6475-6479.

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(1049) Movement-related change of electrocorticographic activity in human supplementary motor area proper.   Ohara S, Ikeda A, Kunieda T, Yazawa S, Baba K, Nagamine T, Taki W, Hashimoto N, Mihara T and Shibasaki H.   2000.  Brain, volume 123, pages 1203-1215. 

(1050) Differences in the corticospinal projection from primary motor cortex and supplementary motor area to macaque upper limb motoneurons: an anatomical and electrophysiological study.   Maier MA, Armand J, Kirkwood PA, Yang HW, Davis JN and Lemon RN.   2002.   Cerebral Cortex, volume 12, pages 281-296.

(1051) Activity of primate subgenual cingulate cortex neurons is related to sleep.   Rolls ET, Inoue K and Browning A.   Journal of Neurophysiology, volume 90, pages 134-142.

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(1053) Increased visual after-effects following pattern adaptation in migraine: a lack of intracortical excitation?   Shepherd AJ.   2001.   Brain, volume 124, pages 2310-2318.

(1054) Painful stimuli evoke different stimulus-response functions in the amygdala, prefrontal, insular and somatosensory cortex: a single-trial fMRI study.   Bornhovd K, Quante M, Glauche V, Bromm B, Weiller C and Buchel C.   2002.   Brain, volume 125, pages 1326-1336.

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(1056) Multiwavelength optical intrinsic signal imaging of cortical spreading depression.   Ba AM, Guiou M, Pouratian N, Muthialu A, Rex DE, Cannestra AF, Chen JW and Toga AW.   2002.   Journal of Neurophysiology, volume 88, pages 2726-2735.

(1057) Haemodynamic brain responses to acute pain in humans: sensory and attentional networks.   Peyron R, Garcia-Larrea L, Gregoire MC, Costes N, Convers P, Lavenne F, Mauguiere F, Michel D and Laurent B.   1999.   Brain, volume 122, pages 1765-1780.

(1058) Error monitoring using external feedback: specific roles of the habenular complex, the reward system, and the cingulate motor area revealed by functional magnetic resonance imaging.   Ullsperger M and Von Cramon DY.   2003.   Journal of Neuroscience, volume 23, pages 4308-4314.

(1059) Neural activity in monkey dorsal and ventral cingulate motor areas: comparison with the supplementary motor area.   Russo GS, Backus DA, Ye S and Crutcher MD.   2002.   Journal of Neurophysiology, volume 88, pages 2612-2629.

(1060) Time course of error detection and correction in humans: neurophysiological evidence.   Rodriguez-Fornells A, Kurzbuch AR and Munte TF.   2002.   Journal of Neuroscience, volume 22, pages 9990-9996.

(1061) Stem cells for the treatment of neurological disorders.   Lindvall O and Kokaia Z.  2006.   Nature, volume 441, pages 1094-1096.

(1062) Activity-dependent dynamics and sequestration of proteasomes in dendritic spines.   Bingol B and Schuman EM.   2006.   Nature, volume 441, pages 1144-1148.

(1063) Organization of inputs from cingulate motor areas to basal ganglia in macaque monkey.   Takada M, Tokuno H, Hamada I, Inase M, Ito Y, Imanishi M, Hasegawa N, Akazawa T, Hatanaka N and Nambu A.   2001.   European Journal of Neuroscience, volume 14, pages 1633-1650.

(1064) Short RNAs in environmental adaptation.   Dalmay T.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1579-1585.

(1065) Separate attentional resources for vision and audition.   Alais D, Morrone C and Burr D.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1339-1345.

(1066) An animal model of chronic placental insufficiency: relevance to neurodevelopmental disorders including schizophrenia.   Rehn AE, Van Den Buuse M, Copolov D, Briscoe T, Lambert G and Rees S.   2004.   Neuroscience, volume 129, pages 381-391.    Adolescence at 8 weeks does not generalise to humans.

(1067) Motor inhibition in patients with Gilles de la Tourette syndrome: functional activation patterns as revealed by EEG coherence.   Serrien DJ, Orth M, Evans AH, Lees AJ and Brown P.   2005.   Brain, volume 128, pages 116-125.

(1068) The brain response to personally familiar faces in autism: findings of fusiform activity and beyond.   Pierce K, Haist F, Sedaghat F and Courchesne E.   2004.   Brain, volume 127, pages 2703-2716.

(1069) The amygdala is enlarged in children but not adolescents with autism; the hippocampus is enlarged at all ages.   Schumann CM, Hamstra J, Goodlin-Jones BL, Lotspeich LJ, Kwon H, Buonocore MH, Lammers CR, Reiss AL and Amaral DG.   2004.   Journal of Neuroscience, volume 24, pages 6392-6401.

(1070) Brain asymmetries in autism and developmental language disorder: a nested whole-brain analysis.   Herbert MR, Ziegler DA, Deutsch CK, O'Brien LM, Kennedy DN, Filipek PA, Bakardjiev AI, Hodgson J, Takeoka M, Makris N and Caviness VS Jr.   2005.   Brain, volume 128, pages 213-226.   As the imaging analysis became more precise, the diagnostic boundaries became more blurred.

(1071) "Trans-generational immune priming": specific enhancement of the antimicrobial response in the mealwork beetle, Tenebrio molitor.   Moret Y.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1399-1405.

(1072) Cross-continental differences in patterns of predation: will naive moose in Scandinavia ever learn?   Sand H, Wikenros C, Wabakken P and Liberg O.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1421-1427.

(1073) fMRI correlates of state and trait effects in subjects at genetically enhanced risk of schizophrenia.   Whalley HC, Simonotto E, Flett S, Marshall I, Ebmeier KP, Owens DG, Goddard NH, Johnstone EC and Lawrie SM.   2004.   Brain, volume 127, pages 478-490.

(1074) Human regional cerebral glucose metabolism during non-rapid eye movement sleep in relation to waking.   Nofzinger EA, Buysse DJ, Miewald JM, Meltzer CC, Price JC, Sembrat RC, Ombao H, Reynolds CF, Monk TH, Hall M, Kupfer DJ and Moore RY.   2002.   Brain, volume 125, pages 1105-1115.

(1075) Sleep-dependent theta oscillations in the human hippocampus and neocortex.   Cantero JL, Atienza M, Stickgold R, Kahana MJ, Madsen JR and Kocsis B.   2003.   Journal of Neuroscience, volume 23, pages 10897-10903.

(1076) Cortical and subcortical correlates of electroencephalographic alpha rhythm modulation.   Feige B, Scheffler K, Esposito F, Di Salle F, Hennig J and Seifritz E.   2005.   Journal of Neurophysiology, volume 93, pages 2864-2872.

(1077) The right brain hemisphere is dominant in human infants.   Chiron C, Jambaque I, Nabbout R, Lounes R, Syrota A and Dulac O.   1997.   Brain, volume 120, pages 1057-1065.

(1078) A functional-anatomical model for lip-reading.   Paulesu E, Perani D, Blasi V, Silani G, Borghese AN, De Giovanni U, Sensolo S and Fazio F.   2003.   Journal of Neurophysiology, volume 90, pages 2005-2013.

(1079) Neural correlates of sad feelings in healthy girls.   Levesque J, Joanette Y, Mensour B, Beaudoin G, Leroux JM, Bourgouin P and Beauregard M.   2003.   Neuroscience, volume 121, pages 545-551.

(1080) Synaptic relationships between axon terminals from the mediodorsal thalamic nucleus and gamma-aminobutyric acidergic cortical cells in the prelimbic cortex of the rat.   Kuroda M, Yokofujita J, Oda S and Price JL.   2004.   Journal of Comparative Neurology, volume 477, pages 220-234.

(1081) Impulsivity, time perception, emotion and reinforcement sensivitivity in patients with orbitofrontal cortex lesions.   Berlin HA, Rolls ET and Kischka U.   2004.   Brain, volume 127, pages 1108-1126.

(1082) Dissociable contributions of the human amygdala and orbitofrontal cortex to incentive motivation and goal selection.   Arana FS, Parkinson JA, Hinton E, Holland AJ, Owen AM and Roberts AC.   2003.   Journal of Neuroscience, volume 23, pages 9632-9638.

(1083) Ventromedial frontal cortex mediates affective shifting in humans: evidence from a reversal learning paradigm.   Fellows LK and Farah MJ.   2003.   Brain, volume 126, pages 1830-1837.

(1084) A neural basis for collecting behaviour in humans.   Anderson SW, Damasio H and Damasio AR.   2005.   Brain, volume 128, pages 201-212.

(1085) The connections of the dopaminergic system with the striatum in rats and primates: an analysis with respect to the functional and compartmental organization of the striatum.   Joel D and Weiner I.   2000.   Neuroscience, volume 96, pages 451-474.

(1086) Chronic behavioral stress induces apical dendritic reorganization in pyramidal neurons of the medial prefrontal cortex.   Radley JJ, Sisti HM, Hao J, Rocher AB, McCall T, Hof PR, McEwen BS and Morrison JH.   2004.   Neuroscience, volume 125, pages 1-6.

(1087) Chronic mild stress impact: are females more vulnerable?   Dalla C, Antoniou K, Drossopoulou G, Xagoraris M, Kokras N, Sfikakis A and Papadopoulou-Daifoti Z.   2005.   Neuroscience, volume 135, pages 703-714.

(1088) Attentional selection and action selection in the ventral and orbital prefrontal cortex.   Rushworth MF, Buckley MJ, Gough PM, Alexander IH, Kyriazis D, McDonald KR and Passingham RE.   2005.   Journal of Neuroscience, volume 25, pages 11628-11636.   "Simply increasing the spatial separation between the instructing stimulus led to slower responses." Presumably, this should read "Simply increasing the spatial separation between the instructing stimulus and the action led to slower responses." As well it might. Syntactic ellipsis has the same effect.

(1089) Cerebral changes during performance of overlearned arbitrary visuomotor associations.   Grol MJ, de Lange FP, Verstraten FA, Passingham RE and Toni I.   2006.   Journal of Neuroscience, volume 26, pages 117-125.

(1090) Striatalnigrostriatal pathways in primates form an ascending spiral from the shell to the dorsolateral striatum.   Haber SN, Fudge JL and McFarland NR.   2000.   Journal of Neuroscience, volume 20, pages 2369-2382.   See in particular the diagram on page 2380, in colour.

(1091) Silent plateau potentials, rhythmic bursts, and pacemaker firing: three patterns of activity that coexist in quadristable subthalamic neurons.   Kass JI and Mintz IM.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 183-188.

(1092) Control of the subthalamic innervation of substantia nigra pars reticulata by D1 and D2 dopamine receptors.   Ibanez-Sandoval O, Hernandez A, Floran B, Galarraga E, Tapia D, Valdiosera R, Erlij D, Aceves J and Bargas J.   2006.   Journal of Neurophysiology, volume 95, pages 1800-1811.

(1093) Panic-prone state induced in rats with GABA dysfunction in the dorsomedial hypothalamus is mediated by NMDA receptors.   Johnson PL and Shekhar A.   2006.   Journal of Neuroscience, volume 26, pages 7093-7104.

(1094) Synaptic and extrasynaptic GABA-A and GABA-B receptors in the globus pallidus: an electron microscopic immunogold analysis in monkeys.   Charara A, Pare JF, Levey AI and Smith Y.   2005.   Neuroscience, volume 131, pages 917-933.

(1095) Stimulation of the subthalamic nucleus changes the firing pattern of pallidal neurons.   Hashimoto T, Elder CM, Okun MS, Patrick SK and Vitek JL.   2003.   Journal of Neuroscience, volume 23, pages 1916-1923.

(1096) Lysozyme. A bacteriolytic ferment found normally in tissues and secretions.   Fleming A.   1929.   The Lancet, volume 1, pages 217-220.

(1097) Mandeville's Travels. Texts and Translations. Volume 2.   Letts M.   London: The Hakluyt Society.   1953.    Pages 395-396. "En ce pays et par toute Ynde il y a grant foison de cocodrilles, cest vne maniere de lons serpens, si comme ie vous ay autres fois dit, qui par nuyt habitent en leaue et par iour sur terre es roches et es cannaux, et si ne manguent point par tout lyuer, mais gisent ens es bouues, si comme font serpens.  Ces serpens manguent les gens en plourant: et quant il manguent, il mueuent la massille dessus et non pas celi de dessoubz et si nont point de langue."    Translation, by Maureen Tweddell.    "In this country and throughout India there are many crocodiles, a type of long snake, as I have already mentioned, who live in water at night and during the day on land in rocks and caves, and which don't eat in the light, but lie in mud, as snakes do.  These snakes eat people while crying, and when they eat, they move their upper jaw, not the lower one, and never their tongue."

(1098) New data on the precise location of the lacrimo-muconasal nucleus of the rat.   Insausti R and Gonzalo LM.   1980.   Experientia, volume 36, pages 977-978.

(1099) Central origins of cranial nerve parasympathetic neurons in the rat.   Contreras RJ, Gomez MM and Norgren R.   1980.   Journal of Comparative Neurology, volume 190, pages 373-394.

(1100) Three novel neural pathways to the lacrimal glands of the cat: an investigation with cholera toxin B subunit as a retrograde tracer.   Cheng S-B, Kuchiiwa S, Kuchiiwa T and Nakagawa S.   2000.   Brain Research, volume 873, pages 160-164.

(1101) A direct hypothalamic projection to the superior salivatory nucleus neurons in the rat.   A study using anterograde autoradiographic and retrograde HRP methods.   Hososya Y, Matsushita M and Sugiura Y.   1983.   Brain Research, volume 266, pages 329-333.

(1102) Prolactin and prolactin receptors in the lacrimal gland.   Wood RL, Zhang J, Huang ZM, Gierow JP, Schechter JE, Mircheff AK and Warren DW.   1999.   Experimental Eye Research, volume 69, pages 213-226.

(1103) Imitation dynamics predict vaccinating behaviour.   Bauch CT.   2005.   Proceedings. Biological Sciences / The Royal Society, volume 272, pages 1669-1675.

(1104) Group decision-making in animals.   Conradt L and Roper TJ.   2003.   Nature, volume 421, pages 155-158.

(1105) Dancing for a decision: a matrix model for nest-site choice by honeybees.   Myerscough MR.   2003.   Proceedings. Biological Sciences / The Royal Society, volume 270, pages 577-582.    Comment. How self-organization evolves.   Visscher PK.   2003.   Nature, volume 421, pages 799-780.

(1106) Insect communication: polarized light as a butterfly mating signal.   Sweeney A, Jiggins C and Johnsen S.   2003.   Nature, volume 423, pages 31-32.

(1107) Comparative rates of violence in chimpanzees and humans.   Wrangham RW, WIlson ML and Muller MN.   2006.   Primates, volume 47, pages 14-26.

(1108) Pattern reversal visual evoked responses of V1/V2 and V5/MT as revealed by MEG combined with probabilistic cytoarchitectonic maps.   Barnikol UB, Amunts K, Dammers J, Mohlberg H, Fieseler T, Malikovic A, Zilles K, Niedeggen M and Tass PA.   2006.   Neuroimage, volume 31, pages 86-108.

(1109) Temporal analysis of the flow from v1 to the extrastriate cortex in humans.   Inui K and Kakigi R.   2006.   Journal of Neurophysiology, volume 96, pages 775-784.

(1110) Short blocks from the noncoding parts of the human genome have instances within nearly all known genes and relate to biological processes.   Rigoutsos I, Huynh T, Miranda K, Tsirigos A, McHardy A and Platt D.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 6605-6610.

(1111) What can animal aggression research tell us about human aggression?   Blanchard DC and Blanchard RJ.   2003.   Hormones and Behavior, volume 44, pages 171-177.

(1112) Group selection and kin selection.   Wynne-Edwards VC.   1964.   Nature, volume 201, page 1147.

(1113) Group selection and kin selection.   Maynard Smith J.   1964.   Nature, volume 201, pages 1145-1147.

(1114) An experimental study of group selection.   Wade MJ.   1977.   Evolution, volume 31, pages 134-153.

(1115) Levels of selection, altruism and primate behavior.   Bradley BJ.   1999.   The Quarterly Review of Biology, volume 74, pages 171-194.

(1116) Foraging specialization without relatedness or dominance among co-founding ant queens.   Rissing SW, Pollock GB, Higgins MR, Hagen RH and Roan Smith D.   1989.   Nature, volume 338, pages 420-422.

(1117) Worker nepotism among polygynous ants.   Hannonen M and Sundström L.   2003.   Nature, volume 421, page 910.

(1118) Normalized perfusion MRI to identify common areas of dysfunction: patients with basal ganglia neglect.   Karnath HO, Zopf R, Johannsen L, Fruhmann Berger M, Nagele T and Klose U.   2005.   Brain, volume 128, pages 2462-2469.

(1119) Dynamic and spatial features of the inhibitory pallidal GABAergic synapses.   Rav-Acha M, Sagiv N, Segev I, Bergman H and Yarom Y.   2005.   Neuroscience, volume 135, pages 791-802.

(1120) Oral dyskinesias and histopathological alterations in substantia nigra after long-term haloperidol treatment of old rats.   Andreassen OA, Ferrante RJ, Aamo TO, Beal MF and Jorgensen HA.   2003.   Neuroscience, volume 122, pages 717-725.   What was the association between reduced cell number and atrophic neurons, and haloperidol, as distinct from saline?

(1121) The effect of contrast on the transfer properties of cat retinal ganglion cells.   Shapley RM and Victor JD.   1978.   Journal of Physiology, volume 285, pages 275-298.

(1122) An edge-detection approach to investigating pigeon navigation.   Lau KK, Roberts S, Biro D, Freeman R, Meade J and Guilford T.   2006.   Journal of Theoretical Biology, volume 239, pages 71-78.

(1123) Vibrotactile frequency discrimination in human hairy skin.   Mahns DA, Perkins NM, Sahai V, Robinson L and Rowe MJ.   2006.   Journal of Neurophysiology, volume 95, pages 1442-1450.

(1124) Gustatory neural responses in the medial orbitofrontal cortex of the old world monkey.   Pritchard TC, Edwards EM, Smith CA, Hilgert KG, Gavlick AM, Maryniak TD, Schwartz GJ and Scott TR.   2005.   Journal of Neuroscience, volume 25, pages 6047-6056.

(1125) Projections from orbitofrontal cortex to anterior piriform cortex in the rat suggest a role in olfactory information processing.   Illig KR.   2005.   Journal of Comparative Neurology, volume 488, pages 224-231.

(1126) Heterogeneous distribution of taste cells in facial and vagal nerve-innervated taste buds.   Eram M and Michel WC.   2006.   Neuroscience, volume 138, pages 339-350.

(1127) Beyond the olfactory bulb: an odotopic map in the forebrain.   Nikonov AA, Finger TE and Caprio J.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 18688-18693.

(1128) Neuropeptide Y modulates excitatory synaptic transmission in the olfactory bulb.   Blakemore LJ, Levenson CW and Trombley PQ.   2006.   Neuroscience, volume 138, pages 663-674.

(1129) Afferent connections of the amygdalopiriform transition area in the rat.   Santiago AC and Shammah-Lagnado SJ.   2005.   Journal of Comparative Neurology, volume 489, pages 349-371.

(1130) Insular and gustatory inputs to the caudal ventral striatum in primates.   Fudge JL, Breitbart MA, Danish M and Pannoni V.   2005.   Journal of Comparative Neurology, volume 490, pages 101-118.

(1131) Unconscious processing of orientation and color without primary visual cortex.   Boyer JL, Harrison S and Ro T.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 16875-16879.

(1132) Visibility, visual awareness, and visual masking of simple unattended targets are confined to areas in the occipital cortex beyond human V1/V2.   Tse PU, Martinez-Conde S, Schlegel AA and Macknik SL.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 17178-17183.

(1133) Whorf hypothesis is supported in the right visual field but not the left.   Gilbert AL, Reiger T, Kay P and Ivry RB.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 489-494.

(1134) Top-down facilitation of visual recognition.   Bar M, Kassam KS, Ghuman AS, Boshyan J, Schmidt AM, Dale AM, Hamalainen MS, Marinkovic K, Schacter DL, Rosen BR and Halgren E.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 449-454.

(1135) Development of saccadic suppression in children.   Bruno A, Brambati SM, Perani D and Morrone MC.   2006.   Journal of Neurophysiology, volume 96, pages 1011-1017.

(1136) Demonstration of cue recruitment: change in visual appearance by means of Pavlovian conditioning.   Haijiang Q, Saunders JA, Stone RW and Backus BT.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 483-488.

(1137) Do we know what the early visual system does?   Carandini M, Demb JB, Mante V, Tolhurst DJ, Dan Y, Olshausen BA, Gallant JL and Rust NC.   2005.   Journal of Neuroscience, volume 25, pages 10577-10597.

(1138) Local connections to specific types of layer 6 neurons in the rat visual cortex.   Zarrinpar A and Callaway EM.   2006.   Journal of Neurophysiology, volume 95, pages 1751-1761.

(1139) Acetylcholine release is elicited in the visual cortex, but not in the prefrontal cortex, by patterned visual stimulation: a dual in vivo microdialysis study with functional correlates in the rat brain.   Laplante F, Morin Y, Quirion R and Vaucher E.   2005.   Neuroscience, volume 132, pages 501-510.

(1140) The segregation and integration of colour in motion processing revealed by motion after-effects.   McKeefry DJ, Laviers EG and McGraw PV.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 91-99.

(1141) Visual and saccade related activity in macaque posterior cingulate cortex.   Dean HL, Crowley JL and Platt ML.   2004.   Journal of Neurophysiology, volume 92, pages 3056-3068.

(1142) Allocentric spatial referencing of neuronal activity in macaque posterior cingulate cortex.   Dean HL and Platt ML.   2006.   Journal of Neuroscience, volume 26, pages 1117-1127.

(1143) Crossmodal integration in the primate superior colliculus underlying the preparation and initiation of saccadic eye movements.   Bell AH, Meredith MA, Van Opstal AJ and Munoz DP.   2005.   Journal of Neurophysiology, volume 93, pages 3659-3673.

(1144) Evaluating the operations underlying multisensory integration in the cat superior colliculus.   Stanford TR, Quessy S and Stein BE.   2005.   Journal of Neuroscience, volume 25, pages 6499-6508.

(1145a) Retinal ganglion cells that project to the superior colliculus and pretectum in the macaque monkey.   Perry VH and Cowey A.   1984.   Neuroscience, volume 12, pages 1125-1137.

(1145b) Retinal ganglion cells that project to the dorsal lateral geniculate nucleus in the macaque monkey.   Perry VH, Oehler R and Cowey A.   1984.   Neuroscience, volume 12, pages 1101-1123.

(1146) Homeostatic, circadian, and emotional regulation of sleep.   Saper CB, Cano G and Scammel TE.   2005.   Journal of Comparative Neurology, volume 493, pages 92-98.

(1147) Visual responses of the human superior colliculus: a high resolution functional magnetic resonance imaging study.   Schneider KA and Kastner S.   2005.   Journal of Neurophysiology, volume 94, pages 2491-2503.

(1148) Organization of the feedback pathway from the striate cortex (V1) to the lateral geniculate nucleus (LGN) in the owl monkey (Aotus trivirgatus).   Ichida JM and Casagrande VA.   2002.   Journal of Comparative Neurology, volume 454, pages 272-283.

(1149) Eye-specific effects of binocular rivalry in the human lateral geniculate nucleus.   Haynes JD, Deichmann R and Rees G.   2005.   Nature, volume 438, pages 496-499.

(1150) Spatial distribution of suppressive signals outside the classical receptive-field in lateral geniculate nucleus.   Webb BS, Tinsley CJ, Vincent CJ and Derrington AM.   2005.   Journal of Neurophysiology, volume 94, pages 1789-1797.

(1151) Direction selectivity of neurons in the striate cortex increases as stimulus contrast is decreased.   Peterson MR, Li B and Freeman RD.   2006.   Journal of Neurophysiology, volume 95, pages 2705-2712.

(1152) Two distinct mechanisms of suppression in human vision.   Petrov Y, Carandini M and McKee S.   2005.   Journal of Neuroscience, volume 25, pages 8704-8707.

(1153) The suppressive field of neurons in lateral geniculate nucleus.   Bonin V, Mante V and Carandini M.   2005.   Journal of Neuroscience, volume 25, pages 10844-10856.

(1154) RNA-binding proteins: a lesson in repression.   Wells DG.   2006.   Journal of Neuroscience, volume 26, pages 7135-7138.

(1155) On measuring the perceived onsets of spontaneous actions.   Lau C, Rogers RD and Passingham RE.   2006.   Journal of Neuroscience, volume 26, pages 7265-7271.

(1156) Rapid inactivation of a moth pheromone.   Ishida Y and Leal WS.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 14075-14079.

(1157) Readiness potentials preceding spontaneous motor acts: voluntary vs. involuntary control.   Keller I and Heckhausen H.   1990.   Electroencephalography and Clinical Neurophysiology, volume 76, pages 351-361.

(1158) Representation of future and previous spatial goals by separate neural populations in prefrontal cortex.   Genovesio A, Brasted PJ and Wise SP.   2006.   Journal of Neuroscience, volume 26, pages 7305-7316.   It is questionable to refer to a visual cue as symbolic in an experiment with monkeys. The result that notionally future and previous spatial goals were represented by separate neural populations in the prefrontal cortex was unremarkable.

(1159) The ventral pallidum and hedonic reward: neurochemical maps of sucrose "liking" and food intake.   Smith KS and Berridge KC.   2005.   Journal of Neuroscience, volume 25, pages 8637-8649.

(1160) The rises and falls of disconnection syndromes.   Catani M and Ffytche DH.   2005.   Brain, volume 128, pages 2224-2239.

(1161) Semantic congruity affects numerical judgments similarly in monkeys and humans.   Cantlon JF, Brannon EM.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 16507-16511.

(1162) Neuroanatomy of flying reptiles and implications for flight, posture and behaviour.   Witmer LM, Chatterjee S, Franzosa J and Rowe T.   2003.   Nature, volume 425, pages 950-953.

(1163) Immediate changes in anticipatory activity of caudate neurons associated with reversal of position-reward contingency.   Watanabe K and Hikosaka O.   2005.   Journal of Neurophysiology, volume 94, pages 1879-1887.

(1164) Switching memory systems during learning: changes in patterns of brain acetylcholine release in the hippocampus and striatum in rats.   Chang Q and Gold PE.   2003.   Journal of Neuroscience, volume 23, pages 3001-3005.

(1165) Reappraisal of the motor role of basal ganglia: a functional magnetic resonance image study.   Taniwaki T, Okayama A, Yoshiura T, Nakamura Y, Goto Y, Kira J and Tobimatsu S.   2003.   Journal of Neuroscience, volume 23, pages 3432-3438.   See the diagram on page 3435, explanatory of different cortical inputs in self-initiated and externally triggered movements.

(1166) Spontaneous pallidal neuronal activity in human dystonia: comparison with Parkinson's disease and normal macaque.   Starr PA, Rau GM, Davis V, Marks WJ, Ostrem JL, Simmons D, Lindsey M and Turner RS.   2005.   Journal of Neurophysiology, volume 93, pages 3165-3176.

(1167) Role of external pallidal segment in primate parkinsonism: comparison of the effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonism and lesions of the external pallidal segment.   Soares J, Kliem MA, Betarbet R, Greenamyre JT, Yamamoto B and Wichmann T.   2004.   Journal of Neuroscience, volume 24, pages 6417-6426.

(1168) Pallidal control of substantia nigra dopaminergic neuron firing pattern and its relation to extracellular neostriatal dopamine levels.   Lee CR, Abercrombie ED and Tepper JM.   2004.   Neuroscience, volume 129, pages 481-489.

(1169) Effects of high-frequency stimulation in the internal globus pallidus on the activity of thalamic neurons in the awake monkey.   Anderson ME, Postupna N and Ruffo M.   2003.   Journal of Neurophysiology, volume 89, pages 1150-1160.

(1170) Subthalamic neurons coordinate basal ganglia function through differential neural pathways.   Yasoshima Y, Kai N, Yoshida S, Shiosaka S, Koyama Y, Kayama Y and Kobayashi K.   2005.   Journal of Neuroscience, volume 25, pages 7743-7753.

(1171) Converging language streams in the human temporal lobe.   Spitsyna G, Warren JE, Scott SK, Turkheimer FE and Wise RJ.   2006.   Journal of Neuroscience, volume 26, pages 7328-7336.

(1172) Prefrontal projections to the thalamic reticular nucleus form a unique circuit for attentional mechanisms.   Zikopoulos B and Barbas H.   2006.   Journal of Neuroscience, volume 26, pages 7348-7361.

(1173) The locus ceruleus is involved in the successful retrieval of emotional memories in humans.   Sterpenich V, D'Argembeau A, Desseilles M, Balteau E, Albouy G, Vandewalle G, Degueldre C, Luxen A, Collette F and Maquet P.   2006.   Journal of Neuroscience, volume 26, pages 7416-7423.

(1174) Time course of functional connectivity between dorsal premotor and contralateral motor cortex during movement selection.   Koch G, Franca M, Del Olmo MF, Cheeran B, Milton R, Alvarez Sauco M and Rothwell JC.   2006.   Journal of Neuroscience, volume 26, pages 7452-7459.

(1175) Theta and gamma oscillations predict encoding and retrieval of declarative memory.   Osipova D, Takashima A, Oostenveld R, Fernandez G, Maris E and Jensen O.   2006.   Journal of Neuroscience, volume 26, pages 7523-7531.

(1176) Effects of reward and behavioral context on neural activity in the primate inferior colliculus.   Metzger RR, Greene NT, Porter KK and Groh JM.   2006.   Journal of Neuroscience, volume 26, pages 7468-7476.

(1177) Sparse representations for the cocktail party problem.   Asari H, Pearlmutter BA and Zador AM.   2006.   Journal of Neuroscience, volume 26, pages 7477-7490.

(1178) Cracking the language code: neural mechanisms underlying speech parsing.   McNealy K, Mazziotta JC and Dapretto M.   2006.   Journal of Neuroscience, volume 26, pages 7629-7639.

(1179) Involvement of the anterior cingulate cortex in the expression of remote spatial memory.   Teixeira CM, Pomedli SR, Maei HR, Kee N and Frankland PW.   2006.   Journal of Neuroscience, volume 26, pages 7555-7564.

(1180) The striatofugal fiber system in primates: a reevaluation of its organization based on single-axon tracing studies.   Levesque M and Parent A.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 11888-11893.

(1181) PET in LRRK2 mutations: comparison to sporadic Parkinson's disease and evidence for presymptomatic compensation.   Adams JR, van Netten H, Schulzer M, Mak E, McKenzie J, Strongosky A, Sossi V, Ruth TJ, Lee CS, Farrer M, Gasser T, Uitti RJ, Calne DB, Wszolek ZK and Stoessl AJ.   2005.   Brain, volume 128, pages 2777-2785.

(1182) Definition and novel connections of the entopallium in the pigeon (Columba livia).   Krutzfeldt NO and Wild JM.   2005.   Journal of Comparative Neurology, volume 490, pages 40-56.

(1183) Seasonal change in neuron size and spacing but not neuronal recruitment in a basal ganglia nucleus in the avian song control system.   Thompson CK and Brenowitz EA.   2005.   Journal of Comparative Neurology, volume 481, pages 276-283.

(1184) Evolutionary dynamics of altruism and cheating among social amoebas.   Brannstrom A and Dieckmann U.   2005.   Proceedings. Biological Sciences / The Royal Society, volume 272, pages 1609-1616.

(1185) Reproductive behavior of the asiatic elephant (Elephas maximus maximus L.).   Eisenberg JF, McKay GM and Jainudeen MR.   1971.   Behaviour, volume 38, pages 193-225.

(1186) Distinct basal ganglia territories are engaged in early and advanced motor sequence learning.   Lehericy S, Benali H, Van de Moortele PF, Pelegrini-Issac M, Waechter T, Ugurbil K and Doyon J.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 12566-12571.

(1187) The roles of the caudate nucleus in human classification learning.   Seger CA and Cincotta CM.   2005.   Journal of Neuroscience, volume 25, pages 2941-2951.

(1188) Cognitive strategies dependent on the hippocampus and caudate nucleus in human navigation: variability and change with practice.   Iaria G, Petrides M, Dagher A, Pike B and Bohbot VD.   2003.   Journal of Neuroscience, volume 23, pages 5945-5952.

(1189) Changes in brain cholecystokinin and anxiety-like behavior following exposure of mice to predator odor.   Hebb AL, Zacharko RM, Dominguez H, Laforest S, Gauthier M, Levac C and Drolet G.   2003.   Neuroscience, volume 116, pages 539-551.

(1190) Lesions in the bed nucleus of the stria terminalis disrupt corticosterone and freezing responses elicited by a contextual but not by a specific cue-conditioned fear stimulus.   Sullivan GM, Apergis J, Bush DE, Johnson LR, Hou M and Ledoux JE.   2004.   Neuroscience, volume 128, pages 7-14.

(1191) Stereological analysis of amygdala neuron number in autism.   Schumann CM and Amaral DG.   2006.   Journal of Neuroscience, volume 26, pages 7674-7679.

(1192) Signaling from blood vessels to CNS axons through nitric oxide.   Garthwaite G, Bartus K, Malcolm D, Goodwin D, Kollb-Sielecka M, Dooldeniva C and Garthwaite J.   2006.   Journal of Neuroscience, volume 26, pages 7730-7740.

(1193) Retraction of synapses and dendritic spines induced by off-target effects of RNA interference.   Alvarez VA, Ridenour DA and Sabatini BL.   2006.   Journal of Neuroscience, volume 26, pages 7820-7825.

(1194) Stress-induced alterations in prefrontal cortical dendritic morphology predict selective impairments in perceptual attentional set-shifting.   Liston C, Miller MM, Goldwater DS, Radley JJ, Rocher AB, Hof PR, Morrison JH and McEwen BS.   2006.   Journal of Neuroscience, volume 26, pages 7870-7874.

(1195) Neural basis of embodiment: distinct contributions of temporoparietal junction and extrastriate body area.   Arzy S, Thut G, Mohr C, Michel CM and Blanke O.   2006.   Journal of Neuroscience, volume 26, pages 8074-8081.

(1196) Localization and connectivity of the lateral amygdala in anuran amphibians.   Moreno N and Gonzalez A.   2004.   Journal of Comparative Neurology, volume 479, pages 130-148.

(1197) Avoidance response in goldfish: emotional and temporal involvement of medial and lateral telencephalic pallium.   Portavella M, Torres B and Salas C.   2004.   Journal of Neuroscience, volume 24, pages 2335-2342.

(1198) Identification of the anterior nucleus of the ansa lenticularis in birds as the homolog of the mammalian subthalamic nucleus.   Jiao Y, Medina L, Veenman CL, Toledo C, Puelles L and Reiner A.   2000.   Journal of Neuroscience, volume 20, pages 6998-7010.

(1199) Parent-offspring conflict theory, signaling of need, and weight gain in early life.   Wells JC.   2003.   The Quarterly Review of Biology, volume 78, pages 169-202.

(1200) The central nucleus of the amygdala projection to dopamine subpopulations in primates.   Fudge JL and Haber SN.   2000.   Neuroscience, volume 97, pages 479-494.

(1201) Independent coding of movement direction and reward prediction by single pallidal neurons.   Arkadir A, Morris G, Vaadia E and Bergman H.   2004.   Journal of Neuroscience, volume 24, pages 10047-10056.

(1202) Differential contribution of dopamine D2S and D2L receptors in the modulation of glutamate and GABA transmission in the striatum.   Centonze D, Gubellini P, Usiello A, Rossi S, Tscherter A, Bracci E, Erbs E, Tognazzi N, Bernardi G, Pisani A, Calabresi P and Borrelli E.   2004.   Neuroscience, volume 129, pages 157-166.

(1203) Balance of monosynaptic excitatory and disynaptic inhibitory responses of the globus pallidus induced after stimulation of the subthalamic nucleus in the monkey.   Kita H, Tachibana Y, Nambu A and Chiken S.   2005.   Journal of Neuroscience, volume 25, pages 8611-8619.

(1204) Functional neuroanatomical correlates of hysterical sensorimotor loss.   Vuilleumier P, Chicherio C, Assal F, Schwartz S, Slosman D and Landis T.   2001.   Brain, volume 124, pages 1077-1090.

(1205) Functional specialization of male and female vocal motoneurons.   Yamaguchi A, Kaczmarek LK and Kelley DB.   2003.   Journal of Neuroscience, volume 23, pages 11568-11576.

(1206) Cholinergic regulation of the central nucleus of the amygdala in rats: effects of local microinjections of cholinomimetics and cholinergic antagonists on arousal and sleep.   Sanford LD, Yang L, Tang X, Dong E, Ross RJ and Morrison AR.   2006.   Neuroscience, volume 141, pages 2167-2176.

(1207) The evolution of phenotypic polymorphism: randomized strategies versus evolutionary branching.   Leimar O.   2005.   The American Naturalist, volume 165, pages 669-681.

(1208) Molecular basis for ultraviolet vision in invertebrates.   Salcedo E, Zheng L, Phistry M, Bagg EE and Britt SG.   2003.   Journal of Neuroscience, volume 23, pages 10873-10878.

(1209) The evolution of inaccurate mimics.   Johnstone RA.   2002.   Nature, volume 418, pages 524-526.

(1210) Friendship, cliquishness, and the emergence of cooperation.   Hruschka DJ and Henrich J.   2006.   Journal of Theoretical Biology, volume 239, pages 1-15.

(1211) Models of parent-offspring conflict. V. Effects of the behaviour of the two parents.   Parker GA.   1985.   Animal Behaviour, volume 33, pages 519-533.

(1212) Territorial defense, territory size and population regulation.   Lopez-Sepulcre A and Kokko H.   2005.   The American Naturalist, volume 166, pages 317-329.

(1213) Kinship-based politics and the optimal size of kin groups.   Hammel EA.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 11951-11956.

(1214) Cooperative breeders adjust offspring sex ratios to produce helpful helpers.   Griffin AS, Sheldon BC and West SA.   2005.   The American Naturalist, volume 166, pages 628-632.

(1215) The evolution of worker caste diversity in social insects.   Fjerdingstad EJ and Crozier RH.   2006.   The American Naturalist, volume 167, pages 390-400.

(1216) Helping non-relatives: a role for deceit?   Connor RC and Curry RL.   1995.   Animal Behaviour, volume 49, pages 389-393.

(1217) Possible constraints on adaptive variation in sex ratio at birth in humans and other primates.   James WH.   2006.   Journal of Theoretical Biology, volume 238, pages 383-394.

(1218) An evolutionary theory of the family.   Emlen ST.   1995.   Proceedings of the National Academy of Sciences of the United States of America, volume 92, pages 8092-8099.

(1219) Evolutionary theory and the human family.   Davis JN and Daly M.   1997.   The Quarterly Review of Biology, volume 72, pages 407-435.

(1220) An experimental analysis of a Mother-daughter rank reversal in Japanese macaques (Macaca fuscata).   Chapais B.   1985.   Primates, volume 26, pages 407-423.

(1221) Contribution of feedforward thalamic afferents and corticogeniculate feedback to the spatial summation area of macaque V1 and LGN.   Angelucci A and Sainsbury K.   2006.   Journal of Comparative Neurology, volume 498, pages 330-351.

(1222) Must reliable signals always be costly?   Maynard Smith J.   1994.   Animal Behaviour, volume 47, pages 1115-1120.   Maynard Smith's critique that Zahavi's argument was verbal and that it was hard to see precisely what was being said, could be levelled at this paper, given the lack of biological data.

(1223) The leading eight: social norms that can maintain cooperation by indirect reciprocity.   Ohtsuki H and Iwasa Y.   2006.   Journal of Theoretical Biology, volume 239, pages 435-444.

(1224) The evolution of cooperation.   Sachs JL, Mueller UG, Wilcox TP and Bull JJ.   2004.   The Quarterly Review of Biology, volume 79, pages 135-160.

(1225) Distributed neural representation of expected value.   Knutson B, Taylor J, Kaufman M, Peterson R and Glover G.   2005.   Journal of Neuroscience, volume 25, pages 4806-4812.

(1226) Partner preferences in by-product mutualisms and the case of predator inspection in fish.   Connor RC.   1996.   Animal Behaviour, volume 51, pages 451-454.

(1227) Localization of tactile stimuli depends on conscious detection.   Harris JA, Karlov L and Clifford CW.   2006.   Journal of Neuroscience, volume 26, pages 948-952.   Patients are motivated to retrieve normality, such as detection, if at all possible. Normal subjects prefer to appear in conscious control of their responses.

(1228) A possible unifying principle for mechanosensation.   Kung C.   2005.   Nature, volume 436, pages 647-654.

(1229) Fully tuneable stochastic resonance in cutaneous receptors.   Fallon JB and Morgan DL.   2005.   Journal of Neurophysiology, volume 94, pages 928-933.

(1230) Tactile form and location processing in the human brain.   Van Boven RW, Ingeholm JE, Beauchamp MS, Bikle PC and Ungerleider LG.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 12601-12605.

(1231) Age-related changes in the inhibitory response properties of dorsal cochlear nucleus output neurons: role of inhibitory inputs.   Caspary DM, Schatteman TA and Hughes LF.   2005.   Journal of Neuroscience, volume 25, pages 10952-10959.

(1232) Sensitivity to interaural time differences in the dorsal nucleus of the lateral lemniscus of the unanesthetized rabbit: comparison with other structures.   Kuwada S, Fitzpatrick DC, Batra R and Ostapoff EM.   2006.   Journal of Neurophysiology, volume 95, pages 1309-1322.

(1233) Unexceptional sharpness of frequency tuning in the human cochlea.   Ruggero MA and Temchin AN.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 18614-18619.

(1234) Neuromagnetic indicators of auditory cortical reorganization of tinnitus.   Weisz N, Wienbruch C, Dohrmann K and Elbert T.   2005.   Brain, volume 128, pages 2722-2731.

(1235) New insights into the auditory processing of communicative signals in the HVC of awake songbirds.   George I, Cousillas H, Richard JP and Hausberger M.   2005.   Neuroscience, volume 136, pages 1-14.

(1236) Conditional associative memory for musical stimuli in nonmusicians: implications for absolute pitch.   Bermudez P and Zatorre RJ.   2005.   Journal of Neuroscience, volume 25, pages 7718-7723.

(1237) Nonauditory events of a behavioral procedure activate auditory cortex of highly trained monkeys.   Brosch M, Selezneva E and Scheich H.   2005.   Journal of Neuroscience, volume 25, pages 6797-6806.

(1238) Sensitivity to voice in human prefrontal cortex.   Fecteau S, Armony JL, Joanette Y and Belin P.   2005.   Journal of Neurophysiology, volume 94, pages 2251-2254.

(1239) Mapping auditory core, lateral belt, and parabelt cortices in the human superior temporal gyrus.   Sweet RA, Dorph-Petersen KA and Lewis DA.   2005.   Journal of Comparative Neurology, volume 491, pages 270-289.

(1240) Mapping phantom movement representations in the motor cortex of amputees.   Mercier C, Reilly KT, Vargas CD, Aballea A and Sirigu A.   2006.   Brain, volume 126, pages 2202-2210.

(1241) Neuropsychological and neuroanatomical correlates of perseverative responses in subacute stroke.   Nys GM, van Zandvoort MJ, van der Worp HB, Kappelle LJ and de Haan EH.   2006.   Brain, volume 129, pages 2148-2157.

(1242) Topography of projections from the primary and non-primary auditory cortical areas to the medial geniculate body and thalamic reticular nucleus in the rat.   Kimura A, Donishi T, Okamoto K and Tamai Y.   2005.   Neuroscience, volume 135, pages 1325-1342.

(1243) Encoding of learned importance of sound by magnitude of representational area in primary auditory cortex.   Rutkowski RG and Weinberger NM.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 13664-13669.

(1244) Neurons in the medial nucleus of the trapezoid body and superior paraolivary nucleus of the rat may play a role in sound duration coding.   Kadner A, Kulesza RJ Jr and Berrebi AS.   2006.   Journal of Neurophysiology, volume 95, pages 1499-1508.

(1245) Rapid brain discrimination of sounds of objects.   Murray MM, Camen C, Gonzalez Andino SL, Bovet P and Clarke S.   2006.   Journal of Neuroscience, volume 26, pages 1293-1302.

(1246) Fine functional organization of auditory cortex revealed by Fourier optical imaging.   Kalatsky VA, Polley DB, Merzenich MM, Schreiner CE and Stryker MP.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 13325-13330.

(1247a) Intermodal selective attention in monkeys. I: distribution and timing of effects across visual areas.   Mehta AD, Ulbert I and Schroeder CE.   2000.   Cerebral Cortex, volume 10, pages 343-358.

(1247b) Intermodal selective attention in monkeys. II: physiological mechanisms of modulation.   Mehta AD, Ulbert I and Schroeder CE.   2000.   Cerebral Cortex, volume 10, pages 359-370.

(1248) Involvement of human thalamus in the preparation of self-paced movement.   Paradiso G, Cunic D, Saint-Cyr JA, Hoque T, Lozano AM, Lang AE and Chen R.   2004.   Brain, volume 127, pages 2717-2731.

(1249) Receptive field properties of the macaque second somatosensory cortex: evidence for multiple functional representations.   Fitzgerald PJ, Lane JW, Thakur PH and Hsiao SS.   2004.   Journal of Neuroscience, volume 24, pages 11193-11204.

(1250) Thalamic infarctions cause side-specific suppression of vestibular cortex activations.   Dieterich M, Bartenstein P, Spiegel S, Bense S, Schwaiger M and Brandt T.   2005.   Brain, volume 128, pages 2052-2067.

(1251) Dominance for vestibular cortical function in the non-dominant hemisphere.   Dieterich M, Bense S, Lutz S, Drzezga A, Stephan T, Bartenstein P and Brandt T.   2003.   Cerebral Cortex, volume 13, pages 994-1007.

(1252) Illusory persistence of touch after right parietal damage: neural correlates of tactile awareness.   Schwartz S, Assal F, Valenza N, Seghier ML and Vuilleumier P.   2005.   Brain, volume 128, pages 227-290.

(1253) Detection and masking of spoiled food smells by odor maps in the olfactory bulb.   Takahashi YK, Nagayama S and Mori K.   2004.   Journal of Neuroscience, volume 24, pages 8690-8694.

(1254) Spatial and temporal organization of ensemble representations for different odor classes in the moth antennal lobe.   Lei H, Christensen TA and Hildebrand JG.   2004.   Journal of Neuroscience, volume 24, pages 11108-11119.

(1255a) Effects of functional group position on spatial representations of aliphatic odorants in the rat olfactory bulb.   Johnson BA, Farahbod H, Saber S and Leon M.   2005.   Journal of Comparative Neurology, volume 483, pages 192-204.

(1255b) Interactions between odorant functional group and hydrocarbon structure influence activity in glomerular response modules in the rat olfactory bulb.   Johnson BA, Farahbod H and Leon M.   2005.   Journal of Comparative Neurology, volume 483, pages 205-216.

(1256) Activity properties and location of neurons in the motor thalamus that project to the cortical motor areas in monkeys.   Kurata K.   2005.   Journal of Neurophysiology, volume 94, pages 550-566.

(1257) Neural correlates of social odor recognition and the representation of individual distinctive social odors within entorhinal cortex and ventral subiculum.   Petrulis A, Alvarez P and Eichenbaum H.   2005.   Neuroscience, volume 130, pages 259-274.

(1258) Learning modulation of odor-induced oscillatory responses in the rat olfactory bulb: a correlate of odor recognition?   Martin C, Gervais R Hugues E, Messaoudi B and Ravel N.   2004.   Journal of Neuroscience, volume 24, pages 389-397.

(1259) The receptors and coding logic for bitter taste.   Mueller KL, Hoon MA, Erlenbach I, Chandrashekar J, Zuker CS and Ryba NJ.   2005.   Nature, volume 434, pages 225-229.

(1260) Experience-dependent neural integration of taste and smell in the human brain.   Small DM, Voss J, Mak YE, Simmons KB, Parrish TR and Gitelman DR.   2004.   Journal of Neurophysiology, volume 92, pages 1892-1903.

(1261) Where is the spike generator of the cochlear nerve? Voltage-gated sodium channels in the mouse cochlea.   Hossain WA, Antic SD, Yang Y, Rasband MN and Morest DK.   2005.   Journal of Neuroscience, volume 25, pages 6857-6868.

(1262) Hair bundle heights in the utricle: differences between macular locations and hair cell types.   Xue J and Peterson EH.   2006.   Journal of Neurophysiology, volume 95, pages 171-186.

(1263) Imaging hair cell transduction at the speed of sound: dynamic behavior of mammalian stereocilia.   Fridberger A, Tomo I, Ulfendahl M and Boutet de Monvel J.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 1918-1923.

(1264) Representation in the human brain of food texture and oral fat.   De Araujo IE and Rolls ET.   2004.   Journal of Neuroscience, volume 24, pages 3086-3093.

(1265) Primate insular/opercular taste cortex: neuronal representations of the viscosity, fat texture, grittiness, temperature, and taste of foods.   Verhagen JV, Kadohisa M and Rolls ET.   2004.   Journal of Neurophysiology, volume 92, pages 1685-1689.

(1266) Representation of umami taste in the human brain.   De Araujo IE, Kringelbach ML, Rolls ET and Hobden P.   2003.   Journal of Neurophysiology, volume 90, pages 313-319.

(1267) Sound of silence activates auditory cortex.   Kraemer DJM, Macrae CN, Green AE and Kelley WM.   2005.   Nature, volume 434, page 158.

(1268) Transgeneration memory of stress in plants.   Molinier J, Ries G, Zipfel C and Hohn B.   2006.   Nature, volume 442, pages 1046-1049.

(1269) Reduced mortality selects for family cohesion in a social species.   Griesser M, Nystrand M and Ekman J.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 1881-1886.

(1270) Sham nepotism as a result of intrinsic differences in brood viability in ants.   Holzer B, Kummerli R, Keller L and Chapuisat M.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2049-2052.

(1271) Sexual conflict reduces offspring fitness in zebra finches.   Royle NJ, Hartley IR and Parker GA.   2002.   Nature, volume 416, pages 733-736.

(1272) A UV signal of offspring condition mediates context-dependent parental favouritism.   Bize P, Piault R, Moureau B and Heeb P.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2063-2068.

(1273) Experimental demonstration that offspring sex ratio varies with maternal condition.   Nager RG, Monaghan P, Griffiths R, Houston DC and Dawson R.   1999.   Proceedings of the National Academy of Sciences of the United States of America, volume 96, pages 570-573.

(1274) Increased reproductive effort results in male-biased offspring sex ratio: an experimental study in a species with reversed sexual size dimorphism.   Kalmbach E, Nager RG, Griffiths R and Furness RW.   2001.   Proceedings. Biological Sciences / The Royal Society, volume 268, pages 2175-2179.

(1275) Cortical projection of peripheral vestibular signaling.   Emri M, Kisely M, Lengyel Z, Balkay L, Marian T, Miko L, Berenyi E, Sziklai I, Tron L and Toth A.   2003.   Journal of Neurophysiology, volume 89, pages 2639-2646.

(1276) Vestibulo-reticular projections in adult lamprey: their role in locomotion.   Pflieger JF and Dubuc R.   2004.   Neuroscience, volume 129, pages 817-829.

(1277) Distinct mechanisms for processing spatial sequences and pitch sequences in the human auditory brain.   Warren JD and Griffiths TD.   2003.   Neuroscience, volume 23, pages 5799-5804.

(1278) The role of the insular cortex in pitch pattern perception: the effect of linguistic contexts.   Wong PC, Parsons LM, Martinez M and Diehl RL.   2004.   Journal of Neuroscience, volume 24, pages 9153-9160.

(1279) Selectivity for the spatial and nonspatial attributes of auditory stimuli in the ventrolateral prefrontal cortex.   Cohen YE, Russ BE, Gifford GW 3rd, Kiringoda R and MacLean KA.   2004.   Journal of Neuroscience, volume 24, pages 11307-11316.   An index of validity is required to resolve these contradictory findings.

(1280) Multiple time scales of adaptation in auditory cortex neurons.   Ulanovsky N, Las L, Farkas D and Nelken I.   2004.   Journal of Neuroscience, volume 24, pages 10440-10453.

(1281) Brain structures differ between musicians and non-musicians.   Gaser C and Schlaug G.   2003.   Journal of Neuroscience, volume 23, pages 9240-9245.

(1282) Digit ratio (2D:4D) moderates the impact of sexual cues on men's decisions in ultimatum games.   Van den Bergh B and Dewitte S.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2091-2095.

(1283) Digit length ratios predict reactive aggression in women, but not in men.   Benderlioglu Z and Nelson RJ.   2004.   Hormones and Behavior, volume 46, pages 558-564.

(1284) Functional imaging with cellular resolution reveals precise microarchitecture in visual cortex.   Ohki K, Chung S, Ch'ng YH, Kara P and Reid RC.   2005.   Nature, volume 433, pages 597-603.

(1285) Short- and long-term effects of cholinergic modulation on gamma oscillations and response synchronization in the visual cortex.   Rodriguez R, Kallenbach U, Singer W and Munk MH.   2004.   Journal of Neuroscience, volume 24, pages 10369-10378.

(1286) Cortical areas involved in object, background, and object-background processing revealed with functional magnetic resonance adaptation.   Goh JO, Siong SC, Park D, Gutchess A, Hebrank A and Chee MW.   2004.   Journal of Neuroscience, volume 24, pages 10223-10228.

(1287) Sluggish and brisk ganglion cells detect contrast with similar sensitivity.   Xu Y, Dhingra NK, Smith RG and Sterling P.   2005.   Journal of Neurophysiology, volume 93, pages 2388-2395.

(1288) Integration of target and effector information in human posterior parietal cortex for the planning of action.   Medendorp WP, Goltz HC, Crawford JD and Vilis T.   2005.   Journal of Neurophysiology, volume 93, pages 954-962.

(1289) The assessment and analysis of handedness: the Edinburgh Inventory.   Oldfield RC.   1971.   Neuropsychologia, volume 9, pages 97-113.

(1290) FMRI activation in the human frontal eye field is correlated with saccadic reaction time.   Connolly JD, Goodale MA, Goltz HC and Munoz DP.   2005.   Journal of Neurophysiology, volume 94, pages 605-611.

(1291) Functional delineation of the human occipito-temporal areas related to face and scene processing. A PET study.   Nakamura K, Kawashima R, Sato N, Nakamura A, Sugiura M, Kato T, Hatano K, Ito K, Fukuda H, Schormann T and Zilles K.   2000.   Brain, volume 123, pages 1903-1912.

(1292) fMRI -adaptation reveals dissociable neural representations of identity and expression in face perception.   Winston JS, Henson RN, Fine-Goulden MR and Dolan RJ.   2004.   Journal of Neurophysiology, volume 92, pages 1830-1839.

(1293) Capacity limit of visual short-term memory in human posterior parietal cortex.   Todd JJ and Marois R.   2004.   Nature, volume 428, pages 751-754.

(1294) Language control in the bilingual brain.   Crinion J, Turner R, Grogan A, Hanakawa T, Noppeney U, Devlin JT, Aso T, Urayama S, Fukuyama H, Stockton K, Usui K, Green DW and Price CJ.   2006.   Science, volume 312, pages 1537-1540.   This was a study of visual working memory, hence the result that neuronal responses within the left caudate were sensitive to changes in the language or the meaning of words; that is, they were sensitive to change.

(1295) Teaching in wild meerkats.   Thornton A and McAuliffe K.   2006.   Science, volume 313, pages 227-229.

(1296) Risky choice and Weber's Law.   Kacelnik A and Brito e Abreu F.   1998.   Journal of Theoretical Biology, volume 194, pages 289-298.

(1297) Framing effects and risky decisions in starlings.   Marsh B and Kacelnik A.   2002.   Proceedings of the National Academy of Sciences of the United States of America, volume 99, pages 3352-3355.

(1298) Frames, biases and rational decision-making in the human brain.   De Martino B, Kumaran D, Seymour B and Dolan RJ.   2006.   Science, volume 313, pages 684-687.

(1299) Food-caching western scrub-jays keep track of who was watching when.   Dally JM, Emery NJ and Clayton NS.   2006.   Science, volume 312, pages 1662-1665.

(1300) Shared brain areas but not functional connections controlling movement timing and order.   Garraux G, McKinney C, Wu T, Kansaku K, Nolte G and Hallett M.   2005.   Journal of Neuroscience,volume 25, pages 5290-5297.

(1301) Cytoarchitectonic identification and probabilistic mapping of two distinct areas within the anterior ventral bank of the human intraparietal sulcus.   Choi HJ, Zilles K, Mohlberg H, Schleicher A, Fink GR, Armstrong E and Amunts K.   2006.   Journal of Comparative Neurology, volume 495, pages 53-69.

(1302) The white 'comma' as a distractive mark on the wings of comma butterflies.   Olofsson M, Dimitrova M and Wiklund C.   2013.   Animal Behaviour, volume 86, 1325-1331.

(1303) Cerebellar involvement in anticipating the consequences of self-produced actions during bimanual movements.   Diedrichsen J, Verstynen T, Lehman SL and Ivry RB.   2005.   Journal of Neurophysiology, volume 93, pages 801-812.

(1304) Memory trace of motor learning shifts transsynaptically from cerebellar cortex to nuclei for consolidation.   Shutoh F, Ohki M, Kitazwa H, Itohara S and Nagao S.   2006.   Neuroscience, volume 139, pages 767-777.

(1305) Axonal propagation of simple and complex spikes in cerebellar Purkinje neurons.   Khaliq ZM and Raman IM.   2005.   Journal of Neuroscience, volume 25, pages 454-463.

(1306) Intermittent visuomotor processing in the human cerebellum, parietal cortex, and premotor cortex.   Vaillancourt DE, Mayka MM and Corcos DM.   2006.   Journal of Neurophysiology, volume 95, pages 922-931.

(1307) Temporal properties of cerebellar-dependent memory consolidation.   Cooke SF, Attwell PJ and Yeo CH.   2004.   Journal of Neuroscience, volume 24, pages 2934-2941.

(1308) A murine model for neuropsychiatric disorders associated with group A beta-hemolytic streptococcal infection.   Hoffman KL Hornig M, Yaddanapudi K, Jabado O and Lipkin WI.   2004.   Journal of Neuroscience, volume 24, pages 1780-1791.

(1309) Glutamate neurotransmission in the cerebellar interposed nuclei: involvement in classically conditioned eyeblinks and neuronal activity.   Aksenov DP, Serdyukova NA, Bloedel JR and Bracha V.   2005.   Journal of Neurophysiology, volume 93, pages 44-52.   These authors simply reported the findings that they had found surprising, without defensive attempts to retrieve their preconceived ideas.

(1310) Extending the cerebellar Lugaro cell class.   Laine J and Axelrad H.   2002.   Neuroscience, volume 115, pages 363-374.

(1311) Activation of human cerebral and cerebellar cortex by auditory stimulation at 40 Hz.   Pastor MA, Artieda J, Arbizu J, Marti-Climent JM, Penuelas I and Masdeu JC.   2002.   Journal of Neuroscience, volume 22, pages 10501-10506.

(1312) The electrocerebellogram.   Niedermeyer E.   2004.   Clinical EEG and Neuroscience, volume 35, pages 112-115.

(1313) Pedunculopontine tegmental nucleus controls conditioned responses of midbrain dopamine neurons in behaving rats.   Pan WX and Hyland BI.   2005.   Journal of Neuroscience, volume 25, pages 4725-4732.

(1314) Improvement and generalization of arm motor performance through motor imagery practice.   Gentili R, Papaxanthis C and Pozzo T.   2006.   Neuroscience, volume 137, pages 761-772.

(1315) Placebo-induced changes in spinal cord pain processing.   Matre D, Casey KL and Knardahl S.   2006.   Journal of Neuroscience, volume 26, pages 559-563.

(1316) Coordination of locomotion with voluntary movements in humans.   Ivanenko YP, Cappellini G, Dominici N, Poppele RE and Lacquaniti F.   2005.   Journal of Neuroscience, volume 25, pages 7238-7253.   The concept of five basic temporal activation patterns in a variety of locomotion conditions that interact with muscle activity required for a voluntary movement, is arbitrary.

(1317) How to enhance ipsilateral actions of pyramidal tract neurons.   Jankowska E, Cabaj A and Pettersson LG.   2005.   Journal of Neuroscience, volume 25, pages 7401-7405.   Elimination of the spinal actions of contralateral PT fibres contradicts mutual facilitation of actions of ipsilateral and contralateral PT neurons.

(1318) Electrophysiological heterogeneity of spinally-projecting serotonergic and non-serotonergic neurons in the rostral ventromedial medulla.   Zhang L, Sykes KT, Buhler AV and Hammond DL.   2006.   Journal of Neurophysiology, volume 95, pages 1853-1863.

(1319) Visual prey capture in larval zebrafish is controlled by identified reticulospinal neurons downstream of the tectum.   Gahtan E, Tanger P and Baier H.   2005.   Journal of Neuroscience, volume 25, pages 9294-9303.

(1320) A comparison of visceral and somatic pain processing in the human brainstem using functional magnetic resonance imaging.   Dunckley P, Wise RG, Fairhurst M, Hobden P, Aziz Q, Chang L and Tracey I.   2005.   Journal of Neuroscience, volume 25, pages 7333-7341.

(1321) Cholinergic modulation of vibrissal receptive fields in trigeminal nuclei.   Timofeeva E, Dufresne C, Sik A, Zhang ZW and Deschenes M.   2005.   Journal of Neuroscience, volume 25, pages 9135-9143.

(1322) Segmental and laminar organization of the spinothalamic neurons in cat: evidence for at least five separate clusters.   Klop EM, Mouton LJ and Holstege G.   2005.   Journal of Comparative Neurology, volume 493, pages 580-595.

(1323) Afferent projections to the pontine micturition center in the cat.   Kuipers R, Mouton LJ and Holstege G.   2006.   Journal of Comparative Neurology, volume 494, pages 36-53.

(1324) Neurotic and endogenous depression: a phylogenetic view.   Price J.   1968.   British Journal of Psychiatry, volume 114, pages 119-120.

(1325) Changes in the excitability of hindlimb motoneurons during muscular atonia induced by stimluating the pedunculopontine tegmental nucleus in cats.   Takakusaki K, Habaguchi T, Saitoh K and Kohyama J.   2004.   Neuroscience, volume 124, pages 467-480.

(1326) Ultrastructural evidence for a direct excitatory pathway from the nucleus retroambiguus to lateral longissimus and quadratus lumborum motoneurons in the female golden hamster.   Gerrits PO, Mouton LJ, Weerd HD, Georgiadis JR, Krukerink M and Holstege G.   2004.   Journal of Comparative Neurology, volume 480, pages 352-363.

(1327) The neural correlates of motor skill automaticity.   Poldrack RA, Sabb FW, Foerde K, Tom SM, Asarnow RF, Bookheimer SY and Knowlton BJ.   2005.   Journal of Neuroscience, volume 25, pages 5356-5364.

(1328) Shifts of effective connectivity within a language network during rhyming and spelling.   Bitan T, Booth JR, Choy J, Burman DD, Gitelman DR and Mesulam MM.   2005.   Journal of Neuroscience, volume 25, pages 5397-5403.

(1329) Encoding and the durability of episodic memory: a functional magnetic resonance imaging study.   Uncapher MR and Rugg MD.   2005.   Journal of Neuroscience, volume 25, pages 7260-7267.

(1330) Rapid perceptual integration of facial expression and emotional body language.   Meeren HK, van Heijnsbergen CC and de Gelder B.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 16518-16523.

(1331) Concurrent working memory load can reduce distraction.   Kim SY, Kim MS and Chun MM.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 16524-16529.

(1332) Working memory as an emergent property of the mind and brain.   Postle BR.   2006.   Neuroscience, volume 139, pages 23-38.

(1333) Interactions between attention and working memory.   Awh E, Vogel EK and Oh SH.   2006.   Neuroscience, volume 139, pages 201-208.

(1334) Inhibitory coupling specifically generates emergent gamma oscillations in diverse cell types.   Sohal VS and Huguenard JR.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 18638-18643.

(1335) Synchronous dynamic brain networks revealed by magnetoencephalography.   Langheim FJ, Leuthold AC and Georgopoulos AP.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 455-459.

(1336) The spread of attention across modalities and space in a multisensory object.   Busse L, Roberts KC, Crist RE, Weissman DH and Woldorff MG.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 18751-18756.

(1337) Item memory, source memory, and the medial temporal lobe: concordant findings from fMRI and memory-impaired patients.   Gold JJ, Smith CN, Bayley PJ, Shrager Y, Brewer JB, Stark CE, Hopkins RO and Squire LR.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 9351-9356.

(1338) Perfusion functional MRI reveals cerebral blood flow pattern under psychological stress.   Wang J, Rao H, Wetmore GS, Furlan PM, Korczykowski M, Dinges DF and Detre JA.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 17804-17809.

(1339) Steroid receptor coregulator diversity: what can it mean for the stressed brain?   Meijer OC, van der Laan S, Lachize S, Steenbergen PJ and de Kloet ER.   2006.   Neuroscience, volume 138, pages 891-899.

(1340) Individual differences in working memory.   Jarrold C and Towse JN.   2006.   Neuroscience, volume 139, pages 39-50.

(1341) Assessing the working memory network: studies with functional magnetic resonance imaging and structural equation modeling.   Schlosser RG, Wagner G and Sauer H.   2006.   Neuroscience, volume 139, pages 91-103.

(1342) Neuroactive steroids and inhibitory neurotransmission: mechanisms of action and physiological relevance.   Belelli D, Herd MB, Mitchell EA, Peden DR, Vardy AW, Gentet L and Lambert JJ.   2006.   Neuroscience, volume 138, pages 821-829.

(1343) Glucocorticoids interact with emotion-induced noradrenergic activation in influencing different memory functions.   Roozendaal B, Okuda S, de Quervain DJ and McGaugh JL.   2006.   Neuroscience, volume 138, pages 901-910.

(1344) Between-task competition and cognitive control in task switching.   Yeung N, Nystrom LE, Aronson JA and Cohen JD.   2006.   Journal of Neuroscience, volume 26, pages 1429-1438.

(1345) Organ of Corti potentials and the motion of the basilar membrane.   Fridberger A, de Monvel JB, Zheng J, Hu N, Zou Y, Ren T and Nuttall A.   2004.   Journal of Neuroscience, volume 24, pages 10057-10063.

(1346) Cortical feedback depolarization waves: a mechanism of top-down influence on early visual areas.   Roland PE, Hanazawa A, Undeman C, Eriksson D, Tompa T, Nakamura H, Valentiniene S and Ahmed B.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 12586-12591.

(1347) Infant brains detect arithmetic errors.   Berger A, Tzur G and Posner MI.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 12649-12653.

(1348) Real-time metabolic imaging.   Golman K, in 't Zandt R and Thaning M.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 11270-11275.

(1349) The influence of meaning on the perception of speech sounds.   Kazanina N, Phillips C and Idsardi W.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 11381-11386.

(1350) Cellular asymmetry and individuality in directional sensing.   Samadani A, Mettetal J and van Oudenaarden A.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 11549-11554.

(1351) Spatial remapping of touch: confusion of perceived stimulus order across hand and foot.   Schicke T and Roder B.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 11808-11813.

(1352) Maintenance of multiple working memory items by temporal segmentation.   Jensen O.   2006.   Neuroscience, volume 139, pages 237-249.

(1353) Distinguishable brain activation networks for short- and long-term motor skill learning.   Floyer-Lea A and Matthews PM.   2005.   Journal of Neurophysiology, volume 94, pages 512-518.

(1354) A functional magnetic resonance imaging study of the effects of pergolide, a dopamine receptor agonist, on component processes of working memory.   Gibbs SE and D'Esposito M.   2006.   Neuroscience, volume 139, pages 359-371.

(1355) Attention lights up new object representations before the old ones fade away.   Khayat PS, Spekreijse H and Roelfsema PR.   2006.   Journal of Neuroscience, volume 26, pages 138-142.

(1356) Noradrenergic modulation of emotion-induced forgetting and remembering.   Hurlemann R, Hawellek B, Matusch A, Kolsch H, Wollersen H, Madea B, Vogeley K, Maier W and Dolan RJ.   2005.   Journal of Neuroscience, volume 25, pages 6343-6349.

(1357) Database and tools for analysis of topographic organization and map transformations in major projection systems of the brain.   Bjaalie JG, Leergaard TB, Lillehaug S, Odeh F, Moene IA, Kjode JO and Darin D.   2005.   Neuroscience, volume 136, pages 681-695.

(1358) Neuroactive steroids: old players in a new game.   Melcangi RC and Panzica GC.   2006.   Neuroscience, volume 138, pages 733-739.

(1359) Glycine receptors in CNS neurons as a target for nonretrograde action of cannabinoids.   Lozovaya N, Yatsenko N, Beketov A, Tsintsadze T and Burnashev N.   2005.   Journal of Neuroscience, volume 25, pages 7499-7506.

(1360) Finding neuroelectric activity under magnetic-field oscillations (NAMO) with magnetic resonance imaging in vivo.   Truong TK and Song AW.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 12598-12601.

(1361) Stress and the suppression of subordinate reproduction in cooperatively breeding meerkats.   Young AJ, Carlson AA, Monfort SL, Russell AF, Bennett NC and Clutton-Brock T.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 12005-12010.

(1362) Placental invasiveness mediates the evolution of hybrid inviability in mammals.   Elliot MG and Crespi BJ.   2006.   The American Naturalist, volume 168, pages 114-120.

(1363) Audience effects on food caching in grey squirrels (Sciurus carolinensis): evidence for pilferage avoidance strategies.   Leaver LA, Hopewell L, Caldwell C and Mallarky L.   2007.   Animal Cognition, volume 10, pages 23-27.

(1364) Unifying the theories of inclusive fitness and reciprocal altrusim.   Fletcher JA and Zwick M.   2006.   The American Naturalist, volume 168, pages 252-262.

(1365) Imaging response inhibition in a stop-signal task: neural correlates independent of signal monitoring and post-response processing.   Li CS, Huang C, Constable RT and Sinha R.   2006.   Journal of Neuroscience, volume 26, pages 186-192.

(1366) Strong effects of subphysiological temperature on the function and plasticity of mammalian presynaptic terminals.   Micheva KD and Smith SJ.   2005.   Journal of Neuroscience, volume 25, pages 7481-7488.

(1367) Stress hormones: a link between maternal condition and sex-biased reproductive investment.   Love OP, Chin EH, Wynne-Edwards KE and Williams TD.   2005.   The American Naturalist, volume 166, pages 751-766.

(1368) Dopamine D5 receptor localization on cholinergic neurons of the rat forebrain and diencephalon: a potential neuroanatomical substrate involved in mediating dopaminergic influences on acetylcholine release.   Berlanga ML, Simpson TK and Alcantara AA.   2005.   Journal of Comparative Neurology, volume 492, pages 34-49.

(1369) Coexpression of cholinergic and noradrenergic phenotypes in human and nonhuman autonomic nervous system.   Weihe E, Schutz B, Hartschuh W, Anlauf M, Schafer MK and Eiden LE.   2005.   Journal of Comparative Neurology, volume 492, pages 370-379.

(1370) Pattern-dependent simultaneous plasticity differentially transforms the input-output relationship of a feedforward circuit.   Smith SL and Otis TS.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 14901-14906.

(1371) Localization of the urotensin II receptor in the rat central nervous system.   Jegou S, Cartier D, Dubessy C, Gonzalez BJ, Chatenet D, Tostvint H, Scalbert E, Leprince J, Vaudry H and Lihrmann I.   2006.   Journal of Comparative Neurology, volume 495, pages 21-36.

(1372) Both of us disgusted in My insula: the common neural basis of seeing and feeling disgust.   Wicker B, Keysers C, Plailly J, Royet JP, Gallese V and Rizzolatti G.   2003.   Neuron, volume 40, pages 655-664.

(1373) Early experience in humans is associated with changes in neuropeptides critical for regulating social behavior.   Fries AB, Ziegler TE, Kurian JR, Jacoris S and Pollak SD.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 17237-17240.

(1374) Barrages of synaptic activity control the gain and sensitivity of cortical neurons.   Shu Y, Hasenstaub A, Badoual M, Bal T and McCormick DA.   2003.   Journal of Neuroscience, volume 23, pages 10388-10401.

(1375) Different presynaptic roles of synapsins at excitatory and inhibitory synapses.   Gitler D, Takagishi Y, Feng J, Ren Y, Rodriguiz RM, Wetsel WC, Greengard P and Augustine GJ.   2004.   Journal of Neuroscience, volume 24, pages 11368-11380.

(1376) Long-term potentiation and memory processes in the psychological works of Sigmund Freud and in the formation of neuropsychiatric symptoms.   Centonze D, Siracusano A, Calabresi P and Bernardi G.   2005.   Neuroscience, volume 130, pages 559-565.

(1377) Spiral waves in disinhibited mammalian neocortex.   Huang X, Troy WC, Yang Q, Ma H, Laing CR, Schiff SJ and Wu JY.   2004.   Journal of Neuroscience, volume 24, pages 9897-9902.

(1378) Dynamics of electrosensory feedback: short-term plasticity and inhibition in a parallel fiber pathway.   Lewis JE and Maler L.   2002.   Journal of Neurophysiology, volume 88, pages 1695-1706.

(1379) Inhibiting the expression of a classically conditioned behavior prevents its extinction.   Krupa TJ and Thompson RF.   2003.   Journal of Neuroscience, volume 23, pages 10577-10584.

(1380) Fine temporal resolution of analytic phase reveals episodic synchronization by state transitions in gamma EEGs.   Freeman WJ and Rogers LJ.   2002.   Journal of Neurophysiology, volume 87, pages 937-945.

(1381) Phase precession of medial prefrontal cortical activity relative to the hippocampal theta rhythm.   Jones MW and Wilson MA.   2005.   Hippocampus, volume 15, pages 867-873.

(1382) The theta/gamma discrete phase code occurring during the hippocampal phase precession may be a more general brain coding scheme.   Lisman J.   2005.   Hippocampus, volume 15, pages 913-922.

(1383) Induced theta oscillations mediate large-scale synchrony with mediotemporal areas during recollection in humans.   Guderian S and Duzel E.   2005.   Hippocampus, volume 15, pages 901-912.

(1384) Autoradiography of receptor-activated G-proteins in post mortem human brain.   Rodríguez-Puertas R, González-Maeso J, Meana JJ and Pazos A.   2000.   Neuroscience, volume 96, pages 169-180.

(1385) Fornix lesions decouple the induction of hippocampal arc transcription from behavior but not plasticity.   Fletcher BR, Calhoun ME, Rapp PR and Shapiro ML.   2006.   Journal of Neuroscience, volume 26, pages 1507-1515.

(1386) The anterior intraparietal sulcus mediates grasp execution, independent of requirement to update: new insights from transcranial magnetic stimulation.   Rice NJ, Tunik E and Grafton ST.   2006.   Journal of Neuroscience, volume 26, pages 8176-8182.

(1387) Corticofugal output from the primate somatosensory cortex selectively modulates innocuous and noxious inputs in the rat spinothalamic system.   Monconduit L, Lopez-Avila A, Molat JL, Chalus M and Villanueva L.   2006.   Journal of Neuroscience, volume 26, pages 8441-8450.

(1388) Human hippocampal theta activity during virtual navigation.   Ekstrom A, Caplan JB, Ho E, Shattuck K, Fried I and Kahana MJ.   2005.   Hippocampus, volume 15, pages 881-889.

(1389) Functional connectivity between the red nucleus and the hippocampus supports the role of the hippocampal formation in sensorimotor integration.   Dypvik AT and Bland BH.   2004.   Journal of Neurophysiology, volume 92, pages 2040-2050.

(1390) Cellular networks underlying human spatial navigation.   Ekstrom A, Kahana MJ, Caplan JB, Fields TA, Isham EA, Newman EL and Fried I.   2003.   Nature, volume 425, pages 184-188.

(1391) Inhibition of perforant path input to the CA1 region by serotonin and noradrenaline.   Otmakhova NA, Lewey J, Asrican B and Lisman JE.   2005.   Journal of Neurophysiology, volume 94, pages 1413-1422.

(1392) The role of the ventromedial prefrontal cortex in abstract state-based inference during decision making in humans.   Hampton AN, Bossaerts P and O'Doherty JP.   2006.   Journal of Neuroscience, volume 26, pages 8360-8367.

(1393) Reward-related cortical inputs define a large striatal region in primates that interface with associative cortical connections, providing a substrate for incentive-based learning.   Haber SN, Kim KS, Mailly P and Calzavara R.   2006.   Journal of Neuroscience, volume 26, pages 8368-8376.   Should "interface" be "interfaces"?

(1394) Cerebellar cortical molecular layer inhibition is organized in parasagittal zones.   Gao W, Chen G, Reinert KC and Ebner TJ.   2006.   Journal of Neuroscience, volume 26, pages 8377-8387.

(1395) Nonpharmacological amelioration of age-related learning deficits: the impact of hippocampal {theta}-triggered training.   Asaka Y, Mauldin KN, Griffin AL, Seager MA, Shurell E and Berry SD.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 13284-13288.

(1396) Dual phase and rate coding in hippocampal place cells: theoretical significance and relationship to entorhinal grid cells.   O'Keefe J and Burgess N.   2005.   Hippocampus, volume 15, pages 853-866.

(1397) The human hippocampus: cognitive maps or relational memory?   Kumaran D and Maguire EA.   2005.   Journal of Neuroscience, volume 25, pages 7254-7259.

(1398) Functional connectivity with the hippocampus during successful memory formation.   Ranganath C, Heller A, Cohen MX, Brozinsky CJ and Rissman J.   2005.   Hippocampus, volume 15, pages 997-1005.

(1399) Descending pathways to the sympathetic preganglionic neurons.   Loewy AD, in Progress in Brain Research: descending pathways to the spinal cord, pages 267-277.   Kuypers HGJM and Martin GF, Editors.   Amsterdam: Elsevier.   1982.

(1400) The identification of a brainstem site controlling spinal sexual reflexes in male rats.   Marson L and McKenna KE.   1990.   Brain Research, volume 515, pages 303-308.

(1401) Neural circuitry involved in sexual function.   McKenna KE.   2001.   Journal of Spinal Cord Medicine, volume 24, pages 148-154.

(1402) The nucleus paragigantocellularis lateralis in the rat. Demonstration of afferents by the retrograde transport of horseradish peroxidase.   Andrezik JA, Chan-Palay V and Palay SL.   1981.   Anatomy and Embryology, volume 161, pages 373-390.

(1403) Entorhinal cortex stimulation modulates amygdala and piriform cortex responses to olfactory bulb inputs in the rat.   Mouly AM and Di Scala G.   2006.   Neuroscience, volume 137, pages 1131-1141.

(1404) One month of human memory consolidation enhances retrieval-related hippocampal activity.   Bosshardt S, Degonda N, Schmidt CF, Boesiger P, Nitsch RM, Hock C and Henke K.   2005.   Hippocampus, volume 15, pages 1026-1040.

(1405) Theta rhythm of navigation: link between path integration and landmark navigation, episodic and semantic memory.   Buzsaki G.   2005.   Hippocampus, volume 15, pages 827-840.

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(1407) Voluntary exercise alters the cytoarchitecture of the adult dentate gyrus by increasing cellular proliferation, dendritic complexity, and spine density.   Eadie BD, Redila VA and Christie BR.   2005.   Journal of Comparative Neurology, volume 486, pages 39-47.

(1408) Cardiovascular neurons of brain stem with projections to spinal cord.   Brown DL and Guyenet PG.   1984.   American Journal of Physiology, volume 247, pages R1009-1016.

(1409) Anatomical and physiological observations on supraspinal control of bladder and urethral sphincter muscles in the cat.   Holstege G, Griffiths D, de Wall H and Dalm E.   1986.   Journal of Comparative Neurology, volume 250, pages 449-461.

(1410) Penile blood flow and musculovascular events during sleep-related erections of middle-aged men.   Karacan I, Hirshkowitz M, Salis PJ, Narter E and Safi MF.   1987.   Journal of Urology, volume 138, pages 177-181.

(1411) Location and morphology of parasympathetic preganglionic neurons in the sacral spinal cord of the cat revealed by retrograde axonal transport of horseradish peroxidase.   Nadelhaft I, Degroat WC and Morgan C.   1980.   Journal of Comparative Neurology, volume 193, pages 265-281.

(1412) Response properties and anatomical organization of pontine and medullary units responsive to vaginal stimulation in the cat.   Rose JD.   1975.   Brain Research, volume 97, pages 79-93.

(1413) A PET study exploring the laterality of brainstem activation in migraine using glyceryl trinitrate.   Afridi SK, Matharu MS, Lee L, Kaube H, Friston KJ, Frackowiak RS and Goadsby PJ.   2005.   Brain, volume 128, pages 932-939.

(1414) Electrical coupling between locomotor-related excitatory interneurons in the mammalian spinal cord.   Hinckley CA and Ziskind-Conhaim L.   2006.   Journal of Neuroscience, volume 26, pages 8477-8483.

(1415) Distinct electrical and chemical connectivity maps in the thalamic reticular nucleus: potential roles in synchronization and sensation.   Deleuze C and Huguenard JR.   2006.   Journal of Neuroscience, volume 26, pages 8633-8645.

(1416) From air oscillations to music and speech: functional magnetic resonance imaging evidence for fine-tuned neural networks in audition.   Tervaniemi M, Szameitat AJ, Kruck S, Schroger E, Alter K, De Baene W and Friederici AD.   2006.   Journal of Neuroscience, volume 26, pages 8647-8652.

(1417) Phenotype of striatofugal medium spiny neurons in parkinsonian and dyskinetic nonhuman primates: a call for a reappraisal of the functional organization of the basal ganglia.   Nadjar A, Brotchie JM, Guigoni C, Li O, Zhou SB, Wang GJ, Ravenscroft P, Georges F, Crossman AR and Bezard E.   2006.   Journal of Neuroscience, volume 26, pages 8653-8661.

(1418) Suppressive surrounds and contrast gain in magnocellular-pathway retinal ganglion cells of macaque.   Solomon SG, Lee BB and Sun H.   2006.   Journal of Neuroscience, volume 26, pages 8715-8726.

(1419) Diversity of gain modulation by noise in neocortical neurons: regulation by the slow afterhyperpolarization conductance.   Higgs MH, Slee SJ and Spain WJ.   2006.   Journal of Neuroscience, volume 26, pages 8787-8799.

(1420) Toward a common circle: interhemispheric contextual modulation in human early visual areas.   Ban H, Yamamoto H, Fukunaga M, Nakagoshi A, Umeda M, Tanaka C and Ejima Y.   2006.   Journal of Neuroscience, volume 26, pages 8804-8809.   What about input from the superior colliculi?

(1421) Sparse odor coding in awake behaving mice.   Rinberg D, Koulakov A and Gelperin A.   2006.   Journal of Neuroscience, volume 26, pages 8857-8865.

(1422) A natural form of learning can increase and decrease the survival of new neurons in the dentate gyrus.   Olariu A, Cleaver KM, Shore LE, Brewer MD and Cameron HA.   2005.   Hippocampus, volume 15, pages 750-762.

(1423) Is there a link between adult neurogenesis and learning?   Leuner B, Gould E and Shors TJ.   2006.   Hippocampus, volume 16, pages 216-224.

(1424) GABA regulates synaptic integration of newly generated neurons in the adult brain.   Ge S, Goh EL, Sailor KA, Kitabatake Y, Ming GL and Song H.   2006.   Nature, volume 439, pages 589-593.

(1425) Cognitve disorganization in hippocampus: a physiological model of the disorganization in psychosis.   Olypher AV, Klement D and Fenton AA.   2006.   Journal of Neuroscience, volume 26, pages 158-168.   Is coactivity not evidence of organisation? Surely coactivity and oscillations would be expected to correlate.

(1426) Morphological and electrophysiological properties of lateral entorhinal cortex layers II and III principal neurons.   Tahvildari B and Alonso A.   2005.   Journal of Comparative Neurology, volume 491, pages 123-140.

(1427a) Medial septal modulation of the ascending brainstem hippocampal synchronizing pathways in the anesthetized rat.   Jackson J and Bland BH.   2006.   Hippocampus, volume 16, pages 1-10.

(1427b) Medial septal modulation of the ascending brainstem hippocampal synchronizing pathways in the freely moving rat.   Bland BH, Bird J, Jackson J and Natsume K.   2006.   Hippocampus, volume 16, pages 11-19.

(1428) Microstructure of a spatial map in the entorhinal cortex.   Hafting T, Fyhn M, Molden S, Moser M-B and Moser EI.   2005.   Nature, volume 436, pages 801-806.    Comment. Neurons and navigation.   Buzsáki G.   2005.   Nature, volume 436, pages 781-782.

(1429) Morphological and numerical analysis of synaptic interactions between neurons in deep and superficial layers of the entorhinal cortex of the rat.   van Haeften T, Baks-te-Bulte L, Goede PH, Wouterlood FG and Witter MP.   2003.   Hippocampus, volume 13, pages 943-952.

(1430) Differential connections of the perirhinal and parahippocampal cortex with the orbital and medial prefrontal networks in macaque monkeys.   Kondo H, Saleem KJS and Price JL.   2005.   Journal of Comparative Neurology, volume 493, pages 479-509.

(1431) GABAergic signaling to newborn neurons in dentate gyrus.   Wadiche LO, Bromberg DA, Bensen AL and Westbrook GL.   2005.   Journal of Neurophysiology, volume 94, pages 4528-4532.

(1432) Functional maturation of adult-generated granule cells.   Overstreet-Wadiche LS and Westbrook GL.   2006.   Hippocampus, volume 16, pages 208-215.

(1433) Scopolamine reduces persistent activity related to long-term encoding in the parahippocampal gyrus during delayed matching in humans.   Schon K, Atri A, Hasselmo ME, Tricarico MD, LoPresti ML and Stern CE.   2005.   Journal of Neuroscience, volume 25, pages 9112-9123.

(1434) Influence of path integration vs. environmental orientation on place cell remapping between visually identical environments.   Fuhs MC, Vanrhoads SR, Casale AE, McNaughton B and Touretzky DS.   2004.   Journal of Neurophysiology, volume 94, pages 2603-2616.

(1435) Self-motion and the origin of differential spatial scaling along the septo-temporal axis of the hippocampus.   Maurer AP, Vanrhoads SR, Sutherland GR, Lipa P and McNaughton BL.   2005.   Hippocampus, volume 15, pages 841-852.

(1436) Age-associated alterations of hippocampal place cells are subregion specific.   Wilson IA, Ikonen S, Gallagher M, Eichenbaum H and Tanila H.   2005.   Journal of Neuroscience, volume 25, pages 6877-6886.

(1437) Signal propagation in oblique dendrites of CA1 pyramidal cells.   Migliore M, Ferrante M and Ascoli GA.   2005.   Journal of Neurophysiology, volume 94, pages 4145-4155.

(1438) Social evolution: kin preference in a social microbe.   Mehdiabadi NJ, Jack CN, Farnham TT, Platt TG, Kalla SE, Shaulsky G, Queller DC and Strassman JE.   2006.   Nature, volume 442, pages 881-882.

(1439) Gene expression: long-term gene silencing by RNAi.   Vastenhouw NL, Brunschwig K, Okihara KL, Muller F, Tijsterman M and Plasterk RH.   2006.   Nature, volume 442, page 882.

(1440) Parochial altruism in humans.   Bernhard H, Fischbacher U and Fehr E.   2006.   Nature, volume 442, pages 912-915.

(1441) The cells and logic for mammalian sour taste detection.  Huang AL, Chen X, Hoon MA, Chandrashekar J, Guo W, Trankner D, Ryba NJ and Zuker CS.   2006.   Nature, volume 442, pages 934-938.

(1442) Polysynaptic olfactory pathway to the ipsi- and contralateral entorhinal cortex mediated via the hippocampus.   Uva L and de Curtis M.   2005.   Neuroscience, volume 130, pages 249-258.

(1443) Spatial-specificity of single-units in the hippocampal formation of freely moving homing pigeons.   Siegel JJ, Nitz D and Bingman VP.   2005.   Hippocampus, volume 15, pages 26-40.

(1444) Navigation expertise and the human hippocampus: a structural brain imaging analysis.   McGuire EA, Spiers HJ, Good CJ, Hartley T, Frackowiak RS and Burgess N.   2003.   Hippocampus, volume 13, pages 250-259.

(1445) Dissociable stages of human consolidation and reconsolidation.   Walker MP, Brakefield T, Hobson JA and Stickgold R.   2003.   Nature, volume 425, pages 616-620.

(1446) Unilateral inner ear damage results in lasting changes in hippocampal CA1 field potentials in vitro.   Zheng Y, Kerr DS, Darlington CL and Smith PF.   2003.   Hippocampus, volume 13, pages 873-878.

(1447) Lag-sensitive repetition suppression effects in the anterior parahippocampal gyrus.   Brozinsky CJ, Yonelinas AP, Kroll NE and Ranganath C.   2005.   Hippocampus, volume 15, pages 557-561.   The association of repetition suppression with relatively short repetition intervals is suggestive of refractoriness. Metabolic neuroimagery might be clarificatory.

(1448) Cortico-hippocampal communication by way of parallel parahippocampal-subicular pathways.   Witter MP, Naber PA, van Haeften T, Machielsen WC, Rombouts SA, Barkhof F, Scheltens P and Lopes da Silva FH.   2000.   Hippocampus, volume 10, pages 398-410.

(1449) Neurophysiology of converging synaptic inputs from the rat prefrontal cortex, amygdala, midline thalamus, and hippocampal formation onto single neurons of the caudate/putamen and nucleus accumbens.   Finch DM.   1996.   Hippocampus, volume 6, pages 495-512.

(1450) Projections from the subiculum to the deep layers of the ipsilateral presubicular and entorhinal cortices in the guinea pig.   Sørensen KE and Shipley MT.   1979.   Journal of Comparative Neurology, volume 188, pages 313-334.

(1451) Social insects: cuticular hydrocarbons inform task decisions.   Greene MJ and Gordon DM.   2003.   Nature, volume 423, page 32.

(1452) Learning induces long-term potentiation in the hippocampus.   Whitlock JR, Heynen AJ, Shuler MG, and Bear MF.   2006.   Science, volume 313, pages 1093-1097.

(1453) Hippocampal dysfunction in schizophrenia.   Schmajuk NA.   2001.   Hippocampus, volume 11, pages 599-613.

(1454) Processing content or location: distinct brain activation in a memory task.   Treyer V, Buck A and Schnider A.   2005.   Hippocampus, volume 15, pages 684-689.

(1455) Recollective qualities modulate hippocampal activation during autobiographical memory retrieval.   Addis DR, Moscovitch M, Crawley AP and McAndrews MP.   2004.   Hippocampus, volume 14, pages 752-762.

(1456) What makes the brain's tickers tock.   Lisman J.   1998.   Nature, volume 394, pages 132-133.

(1457) Phase segregation of medial septal GABAergic neurons during hippocampal theta activity.   Borhegyi Z, Varga V, Szilagyi N, Fabo D and Freund TF.   2004.   Journal of Neuroscience, volume 24, pages 8470-8479.

(1458a) Electrophysiology of the mammillary complex in vitro.   I. Tuberomammillary and lateral mammillary neurons.   Llinás RR and Alonso A.   1992.   Journal of Neurophysiology, volume 68, pages 1307-1320.

(1458b) Electrophysiology of the mammillary complex in vitro.   II. Medial mammillary neurons.    Alonso A and Llinás RR.   1992.   Journal of Neurophysiology, volume 68, pages 1321-1331.

(1459) Cognitive motor control in human pre-supplementary motor area studied by subdural recording of discrimination/selection-related potentials.   Ikeda A, Yazawa S, Kunieda T, Ohara S, Terada K, Mikuni N, Nagamine T, Taki W, Kimura J and Shibasaki H.   1999.   Brain, volume 122, pages 915-931.

(1460) Peak firing rates of rat anterodorsal thalamic head direction cells are high during faster passive rotations.   Zugaro MB, Berthoz A and Wiener SI.   2002.   Hippocampus, volume 12, pages 481-486.

(1461) Dynamic interactions between local surface cues, distal landmarks, and intrinsic circuitry in hippocampal place cells.   Knierim JJ.   2002.   Journal of Neuroscience, volume 22, pages 6254-6264.

(1462) Projections from the periamygdaloid cortex to the amygdaloid complex, the hippocampal formation, and the parahippocampal region: a PHA-L study in the rat.   Majak K and Pitkanen A.   2003.   Hippocampus, volume 13, pages 922-942.

(1463) Human hippocampal and parahippocampal activity during visual associative recognition memory for spatial and nonspatial stimulus configurations.   Duzel E, Habib R, Rotte M, Guderian S, Tulving E and Heinze HJ.   2003.   Journal of Neuroscience, volume 23, pages 9439-9444.

(1464) Follow-up study of learning-disabled children treated with neurofeedback or placebo.   Becerra J, Fernandez T, Harmony T, Caballero MI, Garcia F, Fernandez-Bouzas A, Santiago-Rodriguez E and Prado-Alcala RA.   2006.   Clinical EEG and Neuroscience, volume 37, pages 198-203.

(1465) Similar or disparate brain patterns? The intra-personal EEG variability of three women with multiple personality disorder.   Lapointe AR, Crayton JW, DeVito R, Fichtner CG and Konopka LM.   2006.   Clinical EEG and Neuroscience, volume 37, pages 235-242.

(1466) Laminar origin and septotemporal distribution of entorhinal and perirhinal projections to the hippocampus in the cat.   Witter MP and Groenewegen HJ.   1984.   Journal of Comparative Neurology, volume 224, pages 371-385.

(1467a) The organization of the reciprocal connections between the subiculum and the entorhinal cortex in the cat: I. A neuroanatomical tracing study.   van Groen T, van Haren FJ, Witter MP and Groenewegen HJ.   1986.   Journal of Comparative Neurology, volume 250, pages 485-497.

(1467b) Organization of the reciprocal connections between the subiculum and the entorhinal cortex in the cat: II. An electrophysiological study.   van Groen T and Lopes da Silva FH.   1986.   Journal of Comparative Neurology, volume 251, pages 111-120.

(1468a) Connections of the parahippocampal cortex. I. Cortical afferents.   Room P and Groenewegen HJ.   1986.   Journal of Comparative Neurology, volume 251, pages 415-450.

(1468b) Connections of the parahippocampal cortex in the cat. II. Subcortical afferents.   Room P and Groenewegen HJ.   1986.   Journal of Comparative Neurology, volume 251, pages 451-473.

(1468c) Connections of the parahippocampal cortex in the cat. III. Cortical and thalamic efferents.   Witter MP and Groenewegen HJ.   1986.   Journal of Comparative Neurology, volume 252, pages 1-31.

(1468d) Connections of the parahippocampal cortex in the cat. IV. Subcortical efferents.   Witter MP and Groenewegen HJ.   1986.   Journal of Comparative Neurology, volume 252, pages 51-77.

(1468e) Connections of the parahippocampal cortex in the cat. V. Intrinsic connections; comments on input/output connections with the hippocampus.   Witter MP, Room P, Groenewegen HJ and Lohman AHM.   1986.   Journal of Comparative Neurology, volume 252, pages 78-94.

(1469) Neural mechanisms of genetic risk for impulsivity and violence in humans.   Meyer-Lindenberg A, Buckholtz JW, Kolachana B, Hariri AR, Pezawas L, Blasi G, Wabnitz A, Honea R, Verchinski B, Callicott JH, Egan M, Mattay V and Weinberger DR.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 6269-6274.

(1470) A role for the macaque anterior cingulate gyrus in social valuation.   Rudebeck PH, Buckley MJ, Walton ME and Rushworth MF.   2006.   Science, volume 313, pages 1310-1312.

(1471) The primate subthalamic nucleus. I. Functional properties in intact animals.   Wichmann T, Bergman H, and DeLong MR.   1994.   Journal of Neurophysiology, volume 72, pages 494-506.

(1472) Discharge characteristics of neurons in the red nucleus during voluntary gait modifications: a comparison with the motor cortex.   Lavoie S and Drew T.   2002.   Journal of Neurophysiology, volume 88, pages 1791-1814.

(1473) Visually guided movements suppress subthalamic oscillations in Parkinson's disease patients.   Amirnovin R, Williams ZM, Cosgrove GR and Eskandar EN.   2004.   Journal of Neuroscience, volume 24, pages 11302-11306.

(1474) Differential subcellular and subsynaptic distribution of GABA(A) and GABA(B) receptors in the monkey subthalamic nucleus.   Galvan A, Charara A, Pare JF, Levey AI and Smith Y.   2004.   Neuroscience, volume 127, pages 709-721.

(1475) Hippocampal and cortical place cell plasticity: implications for episodic memory.   Frank LM, Brown EN and Stanley GB.   2006.   Hippocampus, volume 16, pages 775-784.

(1476) Behavioral correlates of the distributed coding of spatial context.   Anderson MI, Killing S, Morris C, O'donoghue A, Onviagha D, Stevenson R, Verriotis M and Jeffrey KJ.   Hippocampus, volume 16, pages 730-742.

(1477) Organization of hippocampal cell assemblies based on theta phase precession.   Maurer AP, Cowen SL, Burke SN, Barnes CA and McNaughton BL.   Hippocampus, volume 16, pages 785-794.

(1478) Quantitative analysis of substantia nigra pars reticulata activity during a visually guided saccade task.   Handel A and Glimcher PW.   1999.   Journal of Neurophysiology, volume 82, pages 3458-3475.

(1479) Neuronal activity in the primate substantia nigra pars reticulata during the performance of simple and memory-guided elbow movements.   Wichmann T and Kliem MA.   2004.   Journal of Neurophysiology, volume 91, pages 815-827.

(1480) Basal ganglia and processing of cortical information: functional interactions between trans-striatal and trans-subthalamic circuits in the substantia nigra pars reticulata.   Kolomiets BP, Deniau JM, Glowinski J, and Thierry AM.   2003.   Neuroscience, volume 117, pages 931-938.

(1481) Contextual modulation of substantia nigra pars reticulata neurons.   Handel A and Glimcher PW.   2000.   Journal of Neurophysiology, volume 83, pages 3042-3048.

(1482) Spontaneous and evoked activity of substantia nigra pars reticulata neurons during high-frequency stimulation of the subthalamic nucleus.   Maurice N, Thierry AM, Glowinski J and Deniau JM.   2003.   Journal of Neuroscience, volume 23, pages 9929-9936.

(1483) GABA, not glutamate, controls the activity of substantia nigra reticulata neurons in awake, unrestrained rats.   Windels F and Kiyatkin EA.   2004.   Journal of Neuroscience, volume 24, pages 6751-6754.

(1484) Identification of a subpopulation of substantia nigra pars compacta gamma-aminobutyric acid neurons that is regulated by basal ganglia activity.   Hebb MO and Robertson HA.   2000.   Journal of Comparative Neurology, volume 416, pages 30-44.

(1485) Human GABA A receptors on dopaminergic neurons in the pars compacta of the substantia nigra.   Petri S, Krampfl K, Dengler R, Bufler J, Weindl A and Arzberger T.   2002.   Journal of Comparative Neurology, volume 452, pages 360-366.

(1486) Electrophysiological characteristics of substantia nigra neurons in organotypic cultures: spontaneous and evoked activities.   Rohrbacher J, Ichinohe N and Kitai ST.   2000.   Neuroscience, volume 97, pages 703-714.

(1487) Ventral tegmental nucleus of Gudden: a pontine hippocampal theta generator?   Bassant MH and Poindessous-Jazat F.   2001.   Hippocampus, volume 11, pages 809-813.   Gudden's nucleus is described as dorsal in reference (B).

(1488) Horizontal eye movement networks in primates as revealed by retrograde transneuronal transfer of rabies virus: differences in monosynaptic input to "slow" and "fast" abducens motoneurons.   Ugolini G, Klam F, Doldan Dans M, Dubayle D, Brandi AM, Buttner-Ennever J and Graf W.   2006.   Journal of Comparative Neurology, volume 498, pages 762-785.

(1489) Role of thalamocortical sensory suppression during arousal: focusing sensory inputs in neocortex.   Castro-Alamancos MA.   2002.   Journal of Neuroscience, volume 22, pages 9651-9655.

(1490) The role of thalamic inputs in surround receptive fields of barrel neurons.   Kwegyir-Afful EE, Bruno RM, Simons DJ and Keller A.   2005.   Journal of Neuroscience, volume 25, pages 5926-5934.

(1491) Synaptologic and fine structural features distinguishing a subset of basal forebrain cholinergic neurons embedded in the dense intrinsic fiber network of the caudal extended amygdala.   Loopuijt LD and Zahm DS.   2006.   Journal of Comparative Neurology, volume 498, pages 93-111.

(1492) Mediodorsal thalamic afferents to layer III of the rat prefrontal cortex: synaptic relationships to subclasses of interneurons.   Rotaru DC, Barrionuevo G and Sesack SR.   2005.   Journal of Comparative Neurology, volume 490, pages 220-238.

(1493) GABAA receptor-mediated tonic inhibition in thalamic neurons.   Cope DW, Hughes SW and Crunelli V.   2005.   Journal of Neuroscience, volume 25, pages 11553-11563.

(1494) Asymmetrical modes of visual bottom-up and top-down integration in the thalamic nucleus rotundus of pigeons.   Folta K, Diekamp B and Gunturkun O.   2004.   Journal of Neuroscience, volume 24, pages 9475-9485.

(1495) Hippocampal theta rhythm: a tag for short-term memory.   Vertes RP.   2005.   Hippocampus, volume 15, pages 923-935.

(1496) Subcortical afferents to the lateral mediodorsal thalamus in cynomolgus monkeys.   Erickson SL, Melchitzky DS and Lewis DA.   2004.   Neuroscience, volume 129, pages 675-690.

(1497) Receptive field size and response latency are correlated within the cat visual thalamus.   Weng C, Yeh CI, Stoelzel CR and Alonso JM.   2005.   Journal of Neurophysiology, volume 93, pages 3537-3547.

(1498) Auditory thalamic organization: cellular slabs, dendritic arbors and tectothalamic axons underlying the frequency map.   McMullen NT, Velenovsky DS and Holmes MG.   2005.   Neuroscience, volume 136, pages 927-943.

(1499) Spatial and temporal visual properties of single neurons in the suprageniculate nucleus of the thalamus.   Paroczy Z, Nagy A, Markus Z, Waleszczyk WJ, Wypych M and Benedek G.   2006.   Neuroscience, volume 137, pages 1397-1404.

(1500) Psychophysical elements of place- and modality-specificity in the thalamic somatic sensory nucleus (ventral caudal - Vc) of awake humans.   Patel S, Ohara S, Dougherty PM, Gracely RH and Lenz FA.   2006.   Journal of Neurophysiology, volume 95, pages 646-659.

(1501) The subcortical anatomy of human spatial neglect: putamen, caudate nucleus and pulvinar.   Karnath HO, Himmelbach M and Rorden C.   2002.   Brain, volume 125, pages 350-360.

(1502) Thalamic relay nuclei of the basal ganglia form both reciprocal and nonreciprocal cortical connections, linking multiple frontal cortical areas.   McFarland NR and Haber SN.   2002.   Journal of Neuroscience, volume 22, pages 8117-8132.

(1503) Distinct firing properties of higher order thalamic relay neurons.   Li J, Bickford ME and Guido W.   2003.   Journal of Neurophysiology, volume 90, pages 291-299.

(1504) Limbic thalamic lesions, appetitively motivated discrimination learning, and training-induced neuronal activity in rabbits.   Smith DM, Freeman JH Jr, Nicholson D and Gabriel M.   2002.   Journal of Neuroscience, volume 22, pages 8212-8221.

(1505) Dissociation of spatial-, object-, and sound-coding neurons in the mediodorsal nucleus of the primate thalamus.   Tanibuchi I and Goldman-Rakic PS.   2003.   Journal of Neurophysiology, volume 89, pages 1067-1077.

(1506) Differential distribution of burst and single-spike responses in auditory thalamus.   He J and Hu B.   2002.   Journal of Neurophysiology, volume 88, pages 2152-2156.

(1507) Chronic back pain is associated with decreased prefrontal and thalamic gray matter density.   Apkarian AV, Sosa Y, Sonty S, Levy RM, Harden RN, Parrish TB and Gitelman DR.   2004.   Journal of Neuroscience, volume 24, pages 10410-10415.

(1508) The role of the human thalamus in processing corollary discharge.   Bellebaum C, Daum I, Koch B, Schwarz M and Hoffmann KP.   2005.   Brain, volume 128, pages 1139-1154.

(1509) Posture-related oscillations in human cerebellar thalamus in essential tremor are enabled by voluntary motor circuits.   Hua SE and Lenz FA.   2005.   Journal of Neurophysiology, volume 93, pages 117-127.

(1510) Corticothalamic resonance, states of vigilance and mentation.   Steriade M.   2000.   Neuroscience, volume 101, pages 243-276.   See the accessible diagram on page 245.

(1511) Theta activity in neurons and networks of the amygdala related to long-term fear memory.   Pape HC, Narayanan RT, Smid J, Stork O and Seidenbecher T.   2005.   Hippocampus, volume 15, pages 874-880.

(1512) The primate amygdala and reinforcement: a dissociation between rule-based and associatively-mediated memory revealed in neuronal activity.   Wilson FA and Rolls ET.   2005.   Neuroscience, volume 133, pages 1061-1072.

(1513) Unilateral storage of fear memories by the amygdala.   Blair HT, Huynh VK, Vaz VT, Van J, Patel RR, Hiteshi AK, Lee JE and Tarpley JW.   2005.   Journal of Neuroscience, volume 25, pages 4198-4205.

(1514) Role of amygdalo-nigral circuitry in conditioning of a visual stimulus paired with food.   Lee HJ, Groshek F, Petrovich GD, Cantalini JP, Gallagher M and Holland PC.   2005.   Journal of Neuroscience, volume 25, pages 3881-3888.

(1515) Tracking the fear engram: the lateral amygdala is an essential locus of fear memory storage.    Schafe GE, Doyere V and LeDoux JE.   2005.   Journal of Neuroscience, volume 25, pages 10010-10014.   Portended by the sophomoric use of "discreet" for "discrete", the sentence: "Despite being one of the best characterized memory systems of the brain, the question of where fear memories are localized in the brain remains a hotly debated issue." does not specify one of the best characterised memory systems of the brain, perhaps in an attempt to be discreet. The attribution to absent others of hot debate is indiscreet.

(1516) Evidence for stroke-induced neurogenesis in the human brain.   Jin K, Wang X, Xie L, Mao XO, Zhu W, Wang Y, Shen J, Mao Y, Banwait S and Greenberg DA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 13198-13202.

(1517) A repressor complex, AP4 transcription factor and geminin, negatively regulates expression of target genes in nonneuronal cells.   Kim MY, Jeong BC, Lee JH, Kee HJ, Kook H, Kim NS, Kim YH, Kim JK, Ahn KY and Kim KK.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 13074-13079.

(1518) Imagery of voluntary movement of fingers, toes and tongue activates corresponding body-part-specific motor representations.   Ehrsson HH, Geyer S and Naito E.   2003.  Journal of Neurophysiology, volume 90, pages 3304-3316.

(1519) Role of active movement in place-specific firing of hippocampal neurons.   Song EY, Kim YB, Kim YH and Jung MW.   2005.   Hippocampus, volume 15, pages 8-17.

(1520) New vistas on amygdala networks in conditioned fear.   Pare D, Quirk GJ and Ledoux JE.   2004.   Journal of Neurophysiology, volume 92, pages 1-9.

(1521) Stereological estimation of the number of neurons in the human amygdaloid complex.   Schumann CM and Amaral DG.   2005.   Journal of Comparative Neurology, volume 491, pages 320-329.

(1522) Amygdalar and prefrontal pathways to the lateral hypothalamus are activated by a learned cue that stimulates eating.   Petrovich GD, Holland PC and Gallagher M.   2005.   Journal of Neuroscience, volume 25, pages 8295-8302.

(1523) Integrated neural representations of odor intensity and affective valence in human amygdala.   Winston JS, Gottfried JA, Kilner JM and Dolan RJ.   2005.   Journal of Neuroscience, volume 25, pages 8903-8907.

(1524) Patterns of axonal branching of neurons of the substantia nigra pars reticulata and pars lateralis in the rat.   Cebrian C, Parent A and Prensa L.   2005.   Journal of Comparative Neurology, volume 492, pages 349-369.

(1525) Specificity in the projections of the prefrontal and insular cortex to ventral striatopallidum and the extened amygdala.   Reynolds SM and Zahm DS.   2005.   Journal of Neuroscience, volume 25, pages 11757-11767.

(1526) Lesions of the basal amygdala block expression of conditioned fear but not extinction.   Anglada-Figueroa D and Quirk GJ.   2005.   Journal of Neuroscience, volume 25, pages 9680-9685.   The results of BA lesions after training do not warrant a conclusion about the BA on training, specifically that the LA-Ce system is not sufficient for fear acquisition when the BA is present. The change from the past tense to the present tense is defensive of the experimental format.

(1527) Amygdala activity is associated with the successful encoding of item, but not source, information for positive and negative stimuli.   Kensinger EA and Schacter DL.   2006.   Journal of Neuroscience, volume 26, pages 2564-2570.

(1528) A mechanism for impaired fear recognition after amygdala damage.   Adolphs R, Gosselin F, Buchanan TW, Tranel D, Schyns P and Damasio AR.   2005.   Nature, volume 433, pages 68-72.

(1529) The lateral amygdala processes the value of conditioned and unconditioned aversive stimuli.   Blair HT, Sotres-Bayon F, Moita MA and Ledoux JE.   2005.   Neuroscience, volume 133, pages 561-569.

(1530) The organization of projections from the amygdala to visual cortical areas TE and V1 in the macaque monkey.   Freese JL and Amaral DG.   2005.   Journal of Comparative Neurology, volume 486, pages 295-317.

(1531) Temperature sensitivity of dopaminergic neurons of the substantia nigra pars compacta; involvent of TRP channels.   Guatteo E, Chung KK, Bowala TK, Bernardi G, Mercuri NB and Lipski J.   2005.   Journal of Neurophysiology, volume 94, pages 3069-3080.

(1532) Does the amygdala modulate adaptation to repeated stress?   Carter RN, Pinnock SB and Herbert J.   2004.   Neuroscience, volume 126, pages 9-19.

(1533) Central cortical projections to motor and somato-sensory cell groups. An experimental study in the rhesus monkey.   Kuypers HGJM.   1960.   Brain, volume 83, pages 161-184.

(1534) Catechol-O-methyltransferase val158met genotype affects processing of emotional stimuli in the amygdala and prefrontal cortex.   Smolka MN, Schumann G, Wrase J, Grusser SM, Flor H, Mann K, Braus DF, Goldman D, Buchel C and Heinz A.   2005.   Journal of Neuroscience, volume 25, pages 836-842.

(1535) Double dissociation of basolateral and central amygdala lesions on the general and outcome-specific forms of pavlovian-instrumental transfer.   Corbit LH and Balleine BW.   2005.   Journal of Neuroscience, volume 25, pages 962-970.

(1536) Mr Dick the schizophrenic.   Keyte JM and Robinson ML.   1980.   The Dickensian, volume 76, pages 37-39.

(1537) Corticotrophin releasing factor-induced synaptic plasticity in the amygdala translates stress into emotional disorders.   Rainnie DG, Bergeron R, Sajdyk TJ, Patil M, Gehlert DR and Shekhar A.   2004.   Journal of Neuroscience, volume 24, pages 3471-3479.   The doses were infused, not was infused. Also, "...nonanxiety-inducing doses..." should read "...non-anxiety inducing doses...", to be consistent with the later "...anxiety-like responses...".

(1538) Brain oxidation is an initial process in sleep induction.   Ikeda M, Ikeda-Sagara M, Okada T, Clement P, Urade Y, Nagai T, Sugiyama T, Yoshioka T, Honda K and Inoue S.   2005.   Neuroscience, volume 130, pages 1029-1040.

(1539) Sleep-dependent motor memory plasticity in the human brain.   Walker MP, Stickgold R, Alsop D, Gaab N and Schlaug G.   2005.   Neuroscience, volume 133, pages 911-917.

(1540) Motor memory consolidation in sleep shapes more effective neuronal representations.   Fischer S, Nitschke MF, Melchert UH, Erdmann C and Born J.   2005.   Journal of Neuroscience, volume 25, pages 11248-11255.

(1541) Trait-like individual differences in the human sleep electroencephalogram.   Buckelmuller J, Landolt HP, Stassen HH and Achermann P.   2006.   Neuroscience, volume 138, pages 351-356.

(1542) A model of event-related EEG synchronization changes in beta and gamma frequency bands.   Grabska-Barwinska A and Zygierewicz J.   2006.   Journal of Theoretical Biology, volume 238, pages 901-913.

(1543) Phase synchronization between alpha and beta oscillations in the human electroencephalogram.   Nikulin VV and Brismar T.   2006.   Neuroscience, volume 137, pages 647-657.

(1544) Recovery after chronic stress fails to reverse amygdaloid neuronal hypertrophy and enhanced anxiety-like behavior.   Vyas A, Pillai G and Chattarji S.   2004.   Neuroscience, volume 128, pages 667-673.

(1545) Amygdala responses to fearful and happy facial expressions under conditions of binocular suppression.   Williams MA, Morris AP, McGlone F, Abbott DF and Mattingley JB.   2004.   Journal of Neuroscience, volume 24, pages 2898-2904.

(1546) Processing of the arousal of subliminal and supraliminal emotional stimuli by the human amygdala.   Glascher J and Adolphs R.   2003.   Journal of Neuroscience, volume 23, pages 10274-10282.

(1547) Quantification of cholinergic and select non-cholinergic mesopontine neuronal populations in the human brain.   Manaye KF, Zweig R, Wu D, Hersh LB, De Lacalle S, Saper CB and German DC.   1999.   Neuroscience, volume 89, pages 759-770.

(1548) The basal forebrain cholinergic system is involved in rapid nerve growth factor (NGF)-induced plasticity in the barrel cortex of adult rats.   Prakash N, Cohen-Cory S, Penschuck S and Frostig R.   2004.   Journal of Neurophysiology, volume 91, pages 424-437.

(1549) Unconditioned stimulus pathways to the amygdala: effects of posterior thalamic and cortical lesions on fear conditioning.   Lanuza E, Nader K and Ledoux JE.   2004.   Neuroscience, volume 125, pages 305-315.

(1550) Disruption of reconsolidation but not consolidation of auditory fear conditioning by noradrenergic blockade in the amygdala.   Debiec J and Ledoux JE.   2004.   Neuroscience, volume 129, pages 267-272.

(1551) A neural network underlying individual differences in emotion and aggression in male golden hamsters.   David JT, Cervantes MC, Trosky KA, Salinas JA and Delville Y.   2004.   Neuroscience, volume 126, pages 567-578.

(1552) Experimental evolution of phenotypic plasticity: how predictive are cross-environment genetic correlations?   Czesak ME, Fox CW and Wolf JB.   2006.   The American Naturalist, volume 168, pages 323-335.

(1553) Neuronal circuitry and synaptic connectivity of the basal ganglia.   Smith Y, Shink E and Sidibe M.   1998.   Neurosurgery Clinics of North America, volume 9, pages 203-222.

(1554) Models of basal ganglia function and pathophysiology of movement disorders.   Wichmann T and DeLong MR.   1998.   Neurosurgery Clinics of North America, volume 9, pages 223-236.

(1555) Assortative mating for fitness and the evolution of recombination.   Blachford A and Agrawal AF.   2006.   Evolution. International Journal of Organic Evolution, volume 60, pages 1337-1343.

(1556) Pontine maps linking somatosensory and cerebellar cortices are in register with climbing fiber somatotopy.   Odeh F, Ackerley R, Bjaalie JG and Apps R.   2005.   Journal of Neuroscience, volume 25, pages 5680-5690.

(1557) Dopamine-dependent changes in the functional connectivity between basal ganglia and cerebral cortex in humans.   Williams D, Tijssen M, Van Bruggen G, Bosch A, Insola A, Di Lazzaro V, Mazzone P, Oliviero A, Quartarone A, Speelman H and Brown P.   2002.   Brain, volume 125, pages 1558-1569.

(1558) A functional MRI study of automatic movements in patients with Parkinson's disease.   Wu T and Hallett M.   2005.   Brain, volume 128, pages 2250-2259.   This study may not have been the first to demonstrate that patients with Parkinson's disease require more brain activity to compensate for basal ganglia dysfunction in order to perform automatic movements. See reference (55), which was not cited in this study, and which should have been, at the very least, to argue that the movements used in that study were not automatic.

(1559) Making the decision to continue the fight or to flee. An analysis of contests between male Haplochromis burtoni (Pisces).   Mosler H-J.   1985.   Behaviour, volume 92, pages 129-145.

(1560) Vervet monkeys and humans show brain asymmetries for processing conspecific vocalizations, but with opposite patterns of laterality.   Gil-da-Costa R and Hauser MD.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2313-2318.

(1561) Exploration of the neural substrates of executive functioning by functional neuroimaging.   Collette F, Hogge M, Salmon E and Van Der Linden M.   2006.   Neuroscience, volume 139, pages 209-221.

(1562) Visual and oculomotor functions of monkey substantia nigra pars reticulata. IV. Relation of substantia nigra to superior colliculus.   Hikosaka O and Wurtz RH.   1983.   Journal of Neurophysiology, volume 49, pages 1285-1301.

(1563) From nestling calls to fledgling silence: adaptive timing of change in response to aerial alarm calls.   Magrath RD, Platzen D and Kondo J.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2335-2341.

(1564) Disruptive coloration produces camouflage independent of background matching.   Schaefer HM and Stobbe N.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2427-2432.

(1565) Romantic love: an fMRI study of a neural mechanism for mate choice.   Fisher H, Aron A and Brown LL.   2005.   Journal of Comparative Neurology, volume 493, pages 58-62.

(1566) Low-probability transmission of neocortical and entorhinal impulses through the perirhinal cortex.   Pelletier JG, Apergis J and Pare D.   2004.   Journal of Neurophysiology, volume 91, pages 2079-2089.

(1567) Asymmetric functional roles of right and left ventromedial prefrontal cortices in social conduct, decision-making, and emotional processing.   Tranel D, Bechara A and Denburg NL.   2002.   Cortex, volume 38, pages 589-612.

(1568) Personality predicts activity in reward and emotional regions associated with humor.   Mobbs D, Hagan CC, Azim E, Menon V and Reiss AL.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 16502-16506.

(1569) Sex differences in brain activation elicited by humor.   Azim E, Mobbs D, Jo B, Menon V and Reiss AL.   2005.   Proceedings of the National Academy of Sciences of the United States of America, volume 102, pages 16496-16501.

(1570) Stress and the inflammatory response: a review of neurogenic inflammation.   Black PH.   2002.   Brain, Behavior, and Immunity, volume 16, pages 622-653.

(1571) Inflammatory disease as chronic stress.   Shanks N, Harbuz MS, Jessop DS, Perks P, Moore PM and Lightman SL.   1998.   Annals of the New York Academy of Sciences, volume 840, pages 599-607.

(1572) Neuroendocrine and cytokines-induced responses to minutes, hours, and days of mental stress.   Matalka KZ.   2003.   Neuro Endocrinology Letters, volume 24, pages 283-292.

(1573) Cooperation through image scoring in humans.   Wedekind C and Milinski M.   2000.   Science, volume 288, pages 850-852.

(1574) A general model of consensus and accuracy in interpersonal perception.   Kenny DA.   1991.   Psychological Review, volume 98, pages 155-163.

(1575) Perceptual compression of space through position integration.   Roulston BW, Self MW and Zeki S.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2507-2512.

(1576) Overconfidence in war games: experimental evidence on expectations, aggression, gender and testosterone.   Johnson DD, McDermott R, Barrett ES, Cowden J, Wrangham R, McIntyre MH and Peter Rosen S.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2513-2520.

(1577) Transgenerational priming of immunity: maternal exposure to a bacterial antigen enhances offspring humoral immunity.   Grindstaff JL, Hasselquist D, Nilsson JK, Sandell M, Smith HG and Stiernman M.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2551-2557.

(1578) Evolutionary games and population dynamics: maintenance of cooperation in public goods games.   Hauert C, Holmes M and Doebeli M.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2565-2570.

(1579) Self-harm caused by an insect's innate immunity.   Sadd BM and Siva-Jothy MT.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2571-2574.

(1580) Environmental enrichment and voluntary exercise massively increase neurogenesis in the adult hippocampus via dissociable pathways.   Olson AK, Eadie BD, Ernst C and Christie BR.   2006.   Hippocampus, volume 16, pages 250-260.

(1581) Distinct morphological stages of dentate granule neuron maturation in the adult mouse hippocampus.   Zhao C, Teng EM, Summers RG Jr, Ming GL and Gage FH.   2006.   Journal of Neuroscience, volume 26, pages 3-11.

(1582) Dopaminergic substantia nigra neurons project topographically organized to the subventricular zone and stimulate precursor cell proliferation in aged primates.   Freundlieb N, Francois C, Tande D, Oertel WH, Hirsch EC and Hoglinger GU.   2006.   Journal of Neuroscience, volume 26, pages 2321-2325.   Has syntax suffered in translation?

(1583) Hypothalamic paraventricular nucleus neurons regulate medullary catecholamine cell responses to restraint stress.   Dayas CV, Buller KM and Day TA.   2004.   Journal of Comparative Neurology, volume 478, pages 22-34.

(1584) Bipolar affective disorder and high achievement: a familial association.   Coryell W, Endicott J, Keller M, Andreasen N, Grove W, Hirschfeld RM and Scheftner W.   1989.   American Journal of Psychiatry, volume 146, pages 983-988.

(1585) Frontotemporal and dopaminergic control of idea generation and creative drive .   Flaherty AW.   2005.   Journal of Comparative Neurology, volume 493, pages 147-153.

(1586) Does brain asymmetry allow efficient performance of simultaneous tasks?   Dadda M and Bisazza A.   2006.   Animal Behaviour, volume 72, pages 523-529.

(1587) Histamine receptors in mammalian retinas.   Gastinger MJ, Barber AJ, Vardi N and Marshak DW.   2006.   Journal of Comparative Neurology, volume 495, pages 658-667.

(1588) Processes that constrain and facilitate the evolution of sexual dimorphism.   Delph LF.   2005.   The American Naturalist, volume 166, supplement 4, pages S1-S4.

(1589) Generalized arousal of mammalian central nervous system.   Pfaff D, Westberg L and Kow L-M.   2005.   Journal of Comparative Neurology, volume 493, pages 86-91.

(1590) Forebrain substrates of reward and motivation.   Wise RA.   2005.   Journal of Comparative Neurology, volume 493, pages 115-121.

(1591) PML inhibits HIF-1alpha translation and neoangiogenesis through repression of mTOR.   Bernardi R, Guernah I, Jin D, Grisendi S, Alimonti A, Teruya-Feldstein J, Cordon-Cardo C, Simon MC, Rafii S and Pandolfi PP.   2006.   Nature, volume 442, pages 779-785.   Although the title of the abstract states that PML inhibits translation through repression of mTOR, in the last sentence of the abstract, PML is identified as a novel suppressor of mTOR.

(1592) Amygdala response to facial expressions reflects emotional learning.   Hooker CI, Germine LT, Knight RT and D'Esposito M.   2006.   Journal of Neuroscience, volume 26, pages 8915-8922.

(1593) Neural representation of task difficulty and decision making during perceptual categorization: a timing diagram.   Philiastides MG, Ratcliff R and Sajda P.   2006.   Journal of Neuroscience, volume 26, pages 8965-8975.

(1594) Encoding difficulty promotes postlearning changes in sleep spindle activity during napping.   Schmidt C, Peigneux P, Muto V, Schenkel M, Knoblauch V, Munch M, de Quervain DJ, Wirz-Justice A and Cajochen C.   2006.   Journal of Neuroscience, volume 26, pages 8976-8982.

(1595) Interoception: the sense of the physiological condition of the body.   Craig AD.   2003.   Current Opinion in Neurobiology, volume 13, pages 500-505.

(1596) Unmyelinated tactile afferents signal touch and project to insular cortex.   Olausson H, Lamarre Y, Backlund H, Morin C, Wallin BG, Starck G, Ekholm S, Strigo I, Worsley K, Vallbo AB and Bushnell MC.   2002.   Nature Neuroscience, volume 5, pages 900-904.

(1597) Lighter or heavier than predicted: neural correlates of corrective mechanisms during erroneously programmed lifts.   Jenmalm P, Schmitz C, Forssberg H and Ehrsson HH.   2006.   Journal of Neuroscience, volume 26, pages 9015-9021.

(1598) Differential encoding mechanisms for subsequent associative recognition and free recall.   Staresina BP and Davachi AL.   2006.   Journal of Neuroscience, volume 26, pages 9162-9172.

(1599) Identification of branching paraventricular neurons of the hypothalamus that project to the rostroventrolateral medulla and spinal cord.   Pyner S and Coote JH.   2000.   Neuroscience, volume 100, pages 549-556.

(1600) Terminals of paraventricular spinal neurones are closely associated with adrenal medullary sympathetic preganglionic neurones: immunocytochemical evidence for vasopressin as a possible neurotransmitter in this pathway.   Motawei K, Pyner S, Ranson RN, Kamel M and Coote JH.   1999.   Experimental Brain Research, volume 126, pages 68-76.

(1601) Measurement of voltage-gated potassium currents in identified spinally-projecting sympathetic neurones of the paraventricular nucleus.   Barrett-Jolley R, Pyner S and Coote JH.   2000.   Journal of Neuroscience Methods, volume 102, pages 25-33.

(1602) Voltage-gated ion channels and hereditary disease.   Lehmann-Horn F and Jurkat-Rott K.   1999.   Physiological Reviews, volume 79, pages 1317-1372.   The statement: "A wonderful example for this development, as evident by this review, is the field of ion channel research which would not be nearly as advanced had it not been for human diseases to clarify.", is an embarrassing mixture of hyperbole, ideas of reference, and teleology.

(1603) Functional imaging and the central control of the bladder.   Kavia RB, Dasgupta R and Fowler CJ.   2005.   Journal of Comparative Neurology, volume 493, pages 27-32.

(1604) Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model.   Bolay H, Reuter U, Dunn AK, Huang Z, Boas DA and Moskowitz MA.   2002.   Nature Medicine, volume 8, pages 136-142.

(1605) Ambiguous coding of stimuli by primary sensory afferents causes a lack of independence in the perception of multiple stimulus attributes.   Carlson BA and Kawasaki M.   2006.   Journal of Neuroscience, volume 26, pages 9173-9183.

(1606) Deciphering the spike train of a sensory neuron: counts and temporal patterns in the rat whisker pathway.   Arabzadeh E, Panzeri S and Diamond ME.   2006.   Journal of Neuroscience, volume 26, pages 9216-9226.

(1607) Integration of exogenous input into a dynamic salience map revealed by perturbing attention.   Balan PF and Gottlieb J.   2006.   Journal of Neuroscience, volume 26, pages 9239-9249.

(1608) Modes of functional connectivity in amygdala pathways dissociates level of awareness for signals of fear.   Williams LM, Das P, Liddell BJ, Kemp AH, Rennie CJ and Gordon E.   2006.   Journal of Neuroscience, volume 26, pages 9264-9271.

(1609) Alpha-band electroencephalographic activity over occipital cortex indexes visuospatial attention bias and predicts visual target detection.   Thut G, Nietzel A, Brandt SA and Pascual-Leone A.   2006.   Journal of Neuroscience, volume 26, pages 9494-9502.

(1610) Context-dependent human extinction memory is mediated by a ventromedial prefrontal and hippocampal network.   Kalisch R, Korenfeld E, Stephan KE, Weiskopf N, Seymour B and Dolan RJ.   2006.   Journal of Neuroscience, volume 26, pages 9503-9511.

(1611) Paradoxical facilitation of object recognition memory after infusion of scopolamine into perirhinal cortex: implications for cholinergic system function.   Winters BD, Saksida LM and Bussy TJ.   2006.   Journal of Neuroscience, volume 26, pages 9520-9529.

(1612) Dissociable systems for gain- and loss-related value predictions and errors of prediction in the human brain.   Yacubian J, Glascher J, Schroeder K, Sommer T, Braus DF, and Buchel C.   2006.   Journal of Neuroscience, volume 26, pages 9530-9537.

(1613) Layer-specific touch-dependent facilitation and depression in the somatosensory cortex during active whisking.   Derdikman D, Yu C, Haidarliu S, Bagdasarian K, Arieli A and Ahissar E.   2006.   Journal of Neuroscience, volume 26, pages 9538-9547.

(1614) Postreactivation glucocorticoids impair recall of established fear memory.   Cai WH, Blundell J, Han J, Greene RW and Powell CM.   2006.   Journal of Neuroscience, volume 26, pages 9560-9566.

(1615) Randomised clinical trial comparing the effects of acupuncture and a newly designed placebo needle in rotator cuff tendinitis.   Kleinhenz J, Streitberger K, Windeler J, Güßbacher A, Mavridis G and Martin E.   1999.   Pain, volume 83, pages 235-241.

(1616) Brain systems mediating cognitive interference by emotional distraction.   Dolcos F and McCarthy G.   2006.   Journal of Neuroscience, volume 26, pages 2072-2079.

(1617) Detecting awareness in the vegetative state.   Owen AM, Coleman MR, Boly M, Davis MH, Laureys S and Pickard JD.   2006.   Science, volume 313, page 1402.   This productive article has evoked four comments to date, 18/03/07: Science, volume 313, pages 1376-1379; Science, volume 313 pages 1395-1396; and two comments in Science, volume 315, page 1221, both with an author reply.

(1618) Responses of primate spinothalamic neurons located in the sacral intermediomedial gray (Stilling's nucleus) to proprioceptive input from the tail.   Milne RJ, Foreman RD and Willis WD.   1982.   Brain Research, volume 234, pages 227-236.

(1619) Temporal and spatial enumeration processes in the primate parietal cortex.   Nieder A, Diester I and Tudusciuc O.   2006.   Science, volume 313, pages 1431-1435.

(1620) Washing away your sins: threatened morality and physical cleansing.   Zhong CB and Lilienquist K.   2006.   Science, volume 313, pages 1451-1452.   In study 4, the act of cleansing could have reduced preparatory motor activity, and thus the probability of any subsequent commitment to motor activity. A control was needed, for motor behaviour that did not cleanse.

(1621) High gamma power is phase-locked to theta oscillations in human neocortex.   Canolty RT, Edwards E, Dalal SS, Soltani M, Nagarajan SS, Kirsch HE, Berger MS, Barbaro NM and Knight RT.   2006.   Science, volume 313, pages 1626-1628.

(1622) Region-specific reduction in entorhinal gamma oscillations and parvalbumin-immunoreactive neurons in animal models of psychiatric illness.   Cunningham MO, Hunt J, Middleton S, LeBeau FE, Gillies MJ, Davies CH, Maycox PR, Whittington MA and Racca C.   2006.   Journal of Neuroscience, volume 26, pages 2767-2776.

(1623) Sexual communication by pheromones in a firefly, Phosphaenus hemipterus (Coleoptera: Lampyridae).   De Cock R and Matthysen E.   2005.   Animal Behaviour, volume 70, pages 807-818.

(1624) Reproductive conflict in social insects: male production by workers in a slave-making ant.   Brunner E, Trindl A, Falk KH, Heinze J and D'Ettorre P.   2005.   Evolution. International Journal of Organic Evolution, volume 59, pages 2480-2482.

(1625) Afferents of the ventral tegmental area in the rat-anatomical substratum for integrative functions.   Geisler S and Zahm DS.   2005.   Journal of Comparative Neurology, volume 490, pages 270-294.

(1626) Topography of cortical projections to the dorsolateral neostriatum in rats: multiple overlapping sensorimotor pathways.   Alloway KD, Lou L, Nwabueze-Ogbo F and Chakrabarti S.   2006.   Journal of Comparative Neurology, volume 499, pages 33-48.

(1627) Differential expression of muscarinic acetylcholine receptors across excitatory and inhibitory cells in visual cortical areas V1 and V2 of the macaque monkey.   Disney AA, Domakonda KV and Aoki C.   2006.   Journal of Comparative Neurology, volume 499, pages 49-63.

(1628) Muscarinic m1 and m2 receptor proteins in local circuit and projection neurons of the primate striatum: anatomical evidence for cholinergic modulation of glutamatergic prefronto-striatal pathways.   Alcantara AA, Mrzljak L, Jakab RL, Levey AI, Hersch SM and Goldman-Rakic PS.   2001.   Journal of Comparative Neurology, volume 434, pages 445-460.

(1629) Mental models and counterfactual thoughts about what might have been.   Byrne RM.   2002.   Trends in Cognitive Sciences, volume 6, pages 426-431.

(1630) The pathogenesis of clinical depression: stressor- and cytokine-induced alterations of neuroplasticity.   Hayley S, Poulter MO, Merali Z and Anisman H.   2005.   Neuroscience, volume 135, pages 659-678.   Depressive illness may be a correlate, or a cause, of altered neuroplasticity.

(1631) Adaptive gain and the role of the locus coeruleus-norepinephrine system in optimal performance.   Aston-Jones G and Cohen JD.   2005.   Journal of Comparative Neurology, volume 493, pages 99-110.

(1632) Melatonin treatment for age-related insomnia.   Zhdanova IV, Wurtman RJ, Regan MM, Taylor JA, Shi JP and Leclair OU.   2001.   Journal of Clinical Endocrinology and Metabolism, volume 86, pages 4727-4730.

(1633) Dissociation of automatic and strategic lexical-semantics: functional magnetic resonance imaging evidence for differing roles of multiple frontotemporal regions.   Gold BT, Balota DA, Jones SJ, Powell DK, Smith CD and Andersen AH.   2006.   Journal of Neuroscience, volume 26, pages 6523-6532.

(1634) A phylogenetic analysis of sleep architecture in mammals: the integration of anatomy, physiology, and ecology.   Lesku JA, Roth TC 2nd, Amlaner CJ and Lima SL.   2006.   The American Naturalist, volume 168, pages 441-453.

(1635) Can autism speak to neuroscience?   Moldin SO, Rubenstein JL and Hyman SE.   2006.   Journal of Neuroscience, volume 26, pages 6893-6896.

(1636) The developmental neurobiology of autism spectrum disorder.   DiCicco-Bloom E, Lord C, Zwaigenbaum L, Courchesne E, Dager SR, Schmitz C, Schultz RT, Crawley J and Young LJ.   2006.   Journal of Neuroscience, volume 26, pages 6897-6906.

(1637) What is a gene?   Pearson H.   2006.   Nature, volume 441, pages 399-401.

(1638) Escitalopram and paroxetine in the treatment of generalised anxiety disorder.   Baldwin DS, Huusom AK and Maehlum E.   2006.   British Journal of Psychiatry, volume 189, pages 264-272.

(1639) Selfish genes: a green beard in the red fire ant.   Keller L and Ross KG.   1998.   Nature, volume 394, pages 573-575.

(1640) The relationship between migratory behaviour, memory and the hippocampus: an intraspecific comparison.   Pravosudov VV, Kitaysky AS and Omanska A.   2006.   Proceedings. Biological Sciences / The Royal Society, volume 273, pages 2641-2649.

(1641) Projection of the lateral part of the entorhinal area to the hippocampus and fascia dentata.   Simonsen-Hjorth A.   1972.   Journal of Comparative Neurology, volume 146, pages 219-232.

(1642) Epistasis correlates to genomic complexity.   Sanjuan R and Elena SF.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 14402-14405.

(1643) Differences in vertebrate microRNA expression.   Ason B, Darnell DK, Wittbrodt B, Berezikov E, Kloosterman WP, Wittbrodt J, Antin PB and Plasterk RH.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 14385-14389.

(1644a) Evolution of sex-biased maternal effects in birds: I. Sex-specific resource allocation among simultaneously growing oocytes.   Young RL and Badyaev AV.   2004.   Journal of Evolutionary Biology, volume 1, pages 1355-1366.   The statement: "Male oocytes grew up to five times faster and reached their ovulation size earlier than female oocytes." contradicts the convention that females do not possess a male chromosome.

(1644b) Evolution of sex-biased maternal effects in birds: II. Contrasting sex-specific oocyte clustering in native and recently established populations.   Badyaev AV, Oh KP and Mui R.   2006.   Journal of Evolutionary Biology, volume 19, pages 909-921.

(1644c) Evolution of sex-biased maternal effects in birds: III. Adjustment of ovulation order can enable sex-specific allocation of hormones, carotenoids, and vitamins.   Badyaev AV, Acevedo Seaman D, Navara KJ, Hill GE and Mendonca MT.   2006.   Journal of Evolutionary Biology, volume 19, pages 1044-1057.

(1645) Adaptive sex differences in growth of pre-ovulation oocytes in a passerine bird.   Badyaev AV, Schwabl H, Young RL, Duckworth RA, Navara KJ and Parlow AF.   2005.   Proceedings. Biological Sciences / The Royal Society, volume 272, pages 2165-2172.

(1646) Sex-biased maternal effects reduce ectoparasite-induced mortality in a passerine bird.   Badyaev AV, Hamstra TL, Oh KP and Acevedo Seaman DA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 14406-14411.

(1647) Task-modulated "what" and "where" pathways in human auditory cortex.   Ahveninen J, Jaaskelainen IP, Raij T, Bonmassar G, Devore S, Hamalainen M, Levanen S, Lin FH, Sams M, Shinn-Cunningham BG, Witzel T and Belliveau JW.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 14608-14613.

(1648) Anterior cingulate cortex activity can be independent of response conflict in Stroop-like tasks.   Roelofs A, van Turennout M and Coles MG.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 13884-13889.

(1649) When motion appears stopped: stereo motion standstill.   Tseng CH, Gobell JL, Lu ZL and Sperling G.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 14953-14958.

(1650) Dissociable roles of ventral and dorsal striatum in instrumental conditioning.   O'Doherty J, Davan P, Schultz J, Deichmann R, Friston K and Dolan RJ.    2004.   Science, volume 304, pages 452-454.

(1651) Inhibited and uninhibited infants "grown up": adult amygdalar response to novelty.   Schwartz CE, Wright CI, Shin LM, Kagan J and Rauch SL.   2003.   Science, volume 300, pages 1952-1953.

(1652) A controlled study of behavioral inhibition in children of parents with panic disorder and depression.   Rosenbaum JF, Biederman J, Hirshfeld-Becker DR, Kagan J, Snidman N, Friedman D, Nineberg A, Gallery DJ and Faraone SV.   2000.   American Journal of Psychiatry, volume 157, pages 2002-2010.

(1653) Stability and social-behavioral consequences of toddlers' inhibited temperament and parenting behaviors.   Rubin KH, Burgess KB and Hastings PD.   2002.   Child Development, volume 73, pages 483-495.

(1654) Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version (K-SADS-PL): initial reliability and validity data.   Kaufman J, Birmaher B, Brent D, Rao U, Flynn C, Moreci P, Williamson D and Ryan N.   1997.   Journal of the American Academy of Child and Adolescent Psychiatry, volume 36, pages 980-988.

(1655) The nature of nurture: maternal effects and chromatin remodeling.   Meaney MJ, in Essays in Social Neuroscience, pages 1-14.   Cacioppo JT and Berntson GG, Editors.   Cambridge MA:Bradford Books MIT Press.   2004.

(1656) Adolescent social anxiety as an outcome of inhibited temperament in childhood.   Schwartz CE, Snidman N and Kagan J.   1999.   Journal of the American Academy of Child and Adolescent Psychiatry, volume 38, pages 1008-1015.

(1657) Emotion Explained.   Rolls ET.   Oxford: Oxford University Press.   2005.   The diffuse reticular network is certainly not central to this explanation, and one is left wondering where the author thinks emotions start.

(1658) A behavioral role for feature detection by sensory bursts.   Marsat G and Pollack GS.   2006.   Journal of Neuroscience, volume 26, pages 10542-10547.

(1659) Genome-wide non-mendelian inheritance of extra-genomic information in Arabidopsis.   Lolle SJ, Victor JL, Young JM and Pruitt RE.   2005.   Nature, volume 434, pages 505-509.

(1660) Efferent projections of reuniens and rhomboid nuclei of the thalamus in the rat.   Vertes RP, Hoover WB, Do Valle AC, Sherman A and Rodriguez JJ.   2006.   Journal of Comparative Neurology, volume 499, pages 768-796.

(1661) Fronto-cerebellar systems are associated with infant motor and adult executive functions in healthy adults but not in schizophrenia.   Ridler K, Veijola JM, Tanskanen P, Miettunen J, Chitnis X, Suckling J, Murray GK, Haapea M, Jones PB, Isohanni MK and Bullmore ET.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 15651-15656.

(1662) Human fronto-mesolimbic networks guide decisions about charitable donation.   Moll J, Krueger F, Zahn R, Pardini M, de Oliveira-Souza R and Grafman J.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 15623-15628.

(1663) Facial affect recognition training in autism: can we animate the fusiform gyrus?   Bolte S, Hubl D, Feineis-Matthews S, Prvulovic D, Dierks T and Poustka F.   2006.   Behavioral Neuroscience, volume 120, pages 211-216.

(1664) Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders.   Dapretto M, Davies MS, Pfeifer JH, Scott AA, Sigman M, Bookheimer SY and Jacoboni M.   2006.   Nature Neuroscience, volume 9, pages 28-30.

(1665) Neural correlates of epigenesis.   Canli T, Qiu M, Omura K, Congdon E, Haas BW, Amin Z, Herrmann MJ, Constable RT and Lesch KP.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 16033-16038.   In this study, the neural correlate of epigenesis was subjective.

(1666) A tunable algorithm for collective decision-making.   Pratt SC and Sumpter DJ.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 15906-15910.

(1667) Direct magnetic resonance detection of neuronal electrical activity.   Petridou N, Plenz D, Silva AC, Loew M, Bodurka J and Bandettini PA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 16015-16020.

(1668) Hereditary family signature of facial expression.   Peleg G, Katzir G, Peleg O, Kamara M, Brodsky L, Hel-Or H, Keren D and Nevo E.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 15921-15926.

(1669) Neurocognitive and electrophysiological evidence of altered face processing in parents of children with autism: implications for a model of abnormal development of social brain circuitry in autism.   Dawson G, Webb SJ, Wijsman E, Schellenberg G, Estes A, Munson J and Faja S.   2005.   Development and Psychopathology, volume 17, pages 679-697.

(1670) Social intelligence in the normal and autistic brain: an fMRI study.   Baron-Cohen S, Ring HA, Wheelwright S, Bullmore ET, Brammer MJ, Simmons A and Williams SC.   1999.   European Journal of Neuroscience, volume 11, pages 1891-1898.

(1671) Why the frontal cortex in autism might be talking only to itself: local over-connectivity but long-distance disconnection.   Courchesne E and Pierce K.   2005.   Current Opinion in Neurobiology, volume 15, pages 225-230.

(1672) Explicit and implicit neural mechanisms for processing of social information from facial expressions: a functional magnetic resonance imaging study.   Critchley H, Daly E, Phillips M, Brammer M, Bullmore S, Van Amelsvoort T, Robertson D, David A and Murphy D.   2000.   Human Brain Mapping, volume 9, pages 93-105.

(1673) Coping sense of humor reduces effects of stereotype threat on women's math performance.   Ford TE, Furguson MA, Brooks JL and Hagadone KM.   2004.   Personality and Social Psychology Bulletin, volume 30, pages 643-653.

(1674) Gaze fixation and the neural circuitry of face processing in autism.   Dalton KM, Nacewicz BM, Johnstone T, Schaefer HS, Gernsbacher MA, Goldsmith HH, Alexander AL and Davidson RJ.   2005.   Nature Neuroscience, volume 8, pages 519-526.

(1675) Inadequate cortical feature maps: a neural circuit theory of autism.   Gustafsson L.   1997.   Biological Psychiatry, volume 15, pages 1138-1147.

(1676) Induction of an illusory shadow person.   Arzy S, Seeck M, Ortique S, Spinelli L and Blanke O.   2006.   Nature, volume 443, page 287.

(1677) Evolution of alternative transcriptional circuits with identical logic.   Tsong AE, Tuch BB, Li H and Johnson AD.   2006.   Nature, volume 443, pages 415-420.

(1678) Structural anatomy of empathy in neurodegenerative disease.   Rankin KP, Gorno-Tempini ML, Allison SC, Stanley CM, Glenn S, Weiner MW and Miller BL.   2006.   Brain, volume 129, pages 2945-2956.

(1679) Navigation around London by a taxi driver with bilateral hippocampal lesions.   Maguire EA, Nannery R and Spiers HJ.   2006.   Brain, volume 129, pages 2894-2907.

(1680) Visual fixation patterns during viewing of naturalistic social situations as predictors of social competence in individuals with autism.   Klin A, Jones W, Schultz R, Volkmar F and Cohen D.   2002.   Archives of General Psychiatry, volume 59, pages 809-816.

(1681) Quantifying the phenotype in autism spectrum disorders.   Lord C, Leventhal BL and Cook EH Jr.   2001.   American Journal of Medical Genetics, volume 105, pages 36-38.

(1682) Early regression in social communication in autism spectrum disorders: a CPEA Study.   Luyster R, Richler J, Risi S, Hsu WL, Dawson G, Bernier R, Dunn M, Hepburn S, Hyman SL, McMahon WM, Goudie-Nice J, Minshew N, Rogers S, Sigman M, Spence MA, Goldberg WA, Tager-Flusberg H, Volkmar FR and Lord C.   2005.   Developmental Neuropsychology, volume 27, pages 311-336.

(1683) Ecological units: definitions and application.   Jax K.   2006.   The Quarterly Review of Biology, volume 81, pages 237-258.

(1684) Replicating empirical research in behavioral ecology: how and why it should be done but rarely ever is.   Kelly CD.   2006.   The Quarterly Review of Biology, volume 81, pages 221-236.

(1685) Neural basis of eye gaze processing deficits in autism.   Pelphrey KA, Morris JP and McCarthy G.   2005.   Brain, volume 128, pages 1038-1048.

(1686) Abnormal ventral temporal cortical activity during face discrimination among individuals with autism and Asperger syndrome.   Schultz RT, Gauthier I, Klin A, Fulbright RK, Anderson AW, Volkmar F, Skudlarski P, Lacadie C, Cohen DJ and Gore JC.   2000.   Archives of General Psychiatry, volume 57, pages 331-340.

(1687) Face processing occurs outside the fusiform "face area" in autism: evidence from functional MRI.   Pierce K, Muller RA, Ambrose J, Allen G and Courchesne E.   2001.   Brain, volume 124, pages 2059-2073.

(1688) Use of polysialic acid in repair of the central nervous system.   El Maarouf A, Petridis AK and Rutishauser U.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 16989-16994.

(1689) A gender- and sexual orientation-dependent spatial attentional effect of invisible images.   Jiang Y, Costello P, Fang F, Huang M and He S.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 17048-17052.

(1690) Day-to-day dynamics of experience-cortisol associations in a population-based sample of older adults.   Adam EK, Hawkley LC, Kudielka BM and Cacioppo JT.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 17058-17063.

(1691) The dynamics of Machiavellian intelligence.   Gavrilets S and Vose A.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 16823-16828.

(1692) Neural basis of dyslexia: a comparison between dyslexic and nondyslexic children equated for reading ability.   Hoeft F, Hernandez A, McMillon G, Taylor-Hill H, Martindale JL, Meyler A, Keller TA, Siok WT, Deutsch GK, Just MA, Whitfield-Gabrieli S and Gabrieli JD.   2006.   Journal of Neuroscience, volume 26, pages 10700-10708.

(1693) Methodological considerations on the use of template matching to study long-lasting memory trace replay.   Tatsuno M, Lipa P and McNaughton BL.   2006.   Journal of Neuroscience, volume 26, pages 10727-10742.

(1694) Integration of auditory and visual communication information in the primate ventrolateral prefrontal cortex.   Sugihara T, Diltz MD, Averbeck BB and Romanski LM.   2006.   Journal of Neuroscience, volume 26, pages 11138-11147.

(1695) Neural mechanisms of expert skills in visual working memory.   Moore CD, Cohen MX and Ranganath C.   2006.   Journal of Neuroscience, volume 26, pages 11187-11196.

(1696) Brain regions mediating flexible rule use during development.   Crone EA, Donohue SE, Honomichi R, Wendelken C and Bunge SA.   2006.   Journal of Neuroscience, volume 26, pages 11239-11247.

(1697) Enhanced performance with brain stimulation: attentional shift or visual cue?   Cavanaugh J, Alvarez BD and Wurtz RH.   2006.   Journal of Neuroscience, volume 26, pages 11347-11358.

(1698) Choosing the lesser of two evils, the better of two goods: specifying the roles of ventromedial prefrontal cortex and dorsal anterior cingulate in object choice.   Blair K, Marsh AA, Morton J, Vythilingam M, Jones M, Mondillo K, Pine DC, Drevets WC and Blair JR.   2006.   Journal of Neuroscience, volume 26, pages 11379-11386.

(1699) Weakened center-surround interactions in visual motion processing in schizophrenia.   Tadin D, Kim J, Doop ML, Gibson C, Lappin JS, Blake R and Park S.   2006.   Journal of Neuroscience, volume 26, pages 11403-11412.

(1700) Emotional modulation of pain: is it the sensation or what we recall?   Godinho F, Magnin M, Frot M, Perchet C and Garcia-Larrea L.   2006.   Journal of Neuroscience, volume 26, pages 11454-11461.

(1701) Anterolateral prefrontal cortex mediates the analgesic effect of expected and perceived control over pain.   Wiech K, Kalisch R, Weiskopf N, Pleger B, Stephan KE and Dolan RJ.   2006.   Journal of Neuroscience, volume 26, pages 11501-11509.

(1702) Enhancing cognition after stress with gene therapy.   Nicholas A, Munchoz CD, Ferguson D, Campbell L and Sapolsky R.   2006.   Journal of Neuroscience, volume 26, pages 11637-11643.

(1703) Directional signals in the prefrontal cortex and in area MT during a working memory for visual motion task.   Zaksas D and Pasternak T.   2006.   Journal of Neuroscience, volume 26, pages 11726-11742.

(1704) The biochemical and neuroendocrine bases of the hyperalgesic nocebo effect.   Benedetti F, Amanzio M, Vighetti S and Asteggiano G.   2006.   Journal of Neuroscience, volume 26, pages 12014-12022.

(1705) Boundary completion is automatic and dissociable from shape discrimination.   Murray MM, Imber ML, Javitt DC and Foxe JJ.   2006.   Journal of Neuroscience, volume 26, pages 12043-12054.

(1706) Precise spatial relationships between mossy fibers and climbing fibers in rat cerebellar cortical zones.   Pijpers A, Apps R, Pardoe J, Voogd J and Ruigrok TJ.   2006.   Journal of Neuroscience, volume 26, pages 12067-12080.

(1707) Event-related potential measures of visual working memory.   Drew TW, McCollough AW and Vogel EK.   2006.   Clinical EEG and Neuroscience, volume 37, pages 286-291.

(1708) Electrophysiological measures of familiarity memory.   Mecklinger A.   2006.   Clinical EEG and Neuroscience, volume 37, pages 292-299.

(1709) Electromagnetic correlates of recognition memory processes.   Neufang M, Heinze HJ and Duzel E.   2006.   Clinical EEG and Neuroscience, volume 37, pages 300-308.

(1710) Do I know you? Insights into memory for faces from brain potentials.   Boehm SG and Paller KA.   2006.   Clinical EEG and Neuroscience, volume 37, pages 322-329.

(1711) Error detection, correction, and prevention in the brain: a brief review of data and theories.   van Veen V and Carter CS.   2006.   Clinical EEG and Neuroscience, volume 37, pages 330-335.

(1712) Structural basis for messenger RNA movement on the ribosome.   Yusupova G, Jenner L, Rees B, Moras D and Yusupov M.   2006.   Nature, volume 444, pages 391-394.

(1713) Real-time observation of trigger factor function on translating ribosomes.   Kaiser CM, Chang HC, Agashe VR, Lakshmipathy SK, Etchells SA, Hayer-Hartl M, Hartl FU and Barral JM.   2006.   Nature, volume 444, pages 455-460.

(1714) Cell death in the nervous system.   Bredesen DE, Rao RV and Mehlen P.   2006.   Nature, volume 443, pages 796-802.

(1715) Influence of the thalamus on spatial visual processing in frontal cortex.   Sommer MA and Wurtz RH.   2006.   Nature, volume 444, pages 374-377.

(1716) In vivo enhancer analysis of human conserved non-coding sequences.   Pennacchio LA, Ahituv N, Moses AM, Prabhakar S, Nobrega MA, Shoukry M, Minovitsky S, Dubchak I, Holt A, Lewis KD, Plajzer-Frick I, Akiyama J, De Val S, Afzal V, Black BL, Couronne O, Eisen MB, Visel A and Rubin EM.   2006.   Nature, volume 444, pages 499-502.

(1717) The receptors and cells for mammalian taste.   Chandrashekar J, Hoon MA, Ryba NJ and Zuker CS.   2006.   Nature, volume 444, pages 288-294.

(1718) Comparative chemosensation from receptors to ecology.   Bargmann CI.   2006.   Nature, volume 444, pages 295-301.

(1719) Pheromonal communication in vertebrates.   Brennan PA and Zufall F.   2006.   Nature, volume 444, pages 308-315.

(1720) Smell images and the flavour system in the human brain.   Shepherd GM.   2006.   Nature, volume 444, pages 316-321.

(1721) Global variation in copy number in the human genome.   Redon R, Ishikawa S, Fitch KR, Feuk L, Perry GH, Andrews TD, Fiegler H, Shapero MH, Carson AR, Chen W, Cho EK, Dallaire S, Freeman JL, Gonzalez JR, Gratacos M, Huang J, Kalaitzopoulos D, Komura D, MacDonald JR, Marshall CR, Mei R, Montgomery L, Nishimura K, Okamura K, Shen F, Somerville MJ, Tchinda J, Valsesia A, Woodwark C, Yang F, Zhang J, Zerjal T, Zhang J, Armengol L, Conrad DF, Estivill X, Tyler-Smith C, Carter NP, Aburatani H, Lee C, Jones KW, Scherer SW and Hurles ME.   2006.   Nature, volume 444, pages 444-454.

(1722) Accelerated evolution of conserved noncoding sequences in humans.   Prabhakar S, Noonan JP, Paabo S and Rubin EM.   2006.   Science, volume 314, pages 786.

(1723) Rapid temporal reversal in predator-driven natural selection.   Losos JB, Schoener TW, Langerhans RB and Spiller DA.   2006.   Science, volume 314, page 1111.

(1724) Predictive codes for forthcoming perception in the frontal cortex.   Summerfield C, Egner T, Greene M, Koechlin E, Mangels J and Hirsch J.   2006.   Science, volume 314, pages 1311-1314.

(1725) From grid cells to place cells: a mathematical model.   Solstad T, Moser EI and Einevoll GT.   2006.   Hippocampus, volume 16, pages 1026-1031.

(1726) Retrograde analyses of spinothalamic projections in the macaque monkey: input to posterolateral thalamus.   Craig AD and Zhang ET.   2006.   Journal of Comparative Neurology, volume 499, pages 953-964.

(1727) Retrograde analyses of spinothalamic projections in the macaque monkey: input to ventral posterior nuclei.   Craig AD.   2006.   Journal of Comparative Neurology, volume 499, pages 965-978.

(1728) Amygdala interconnections with the cingulate motor cortex in the rhesus monkey.   Morecraft RJ, McNeal DW, Stilwell-Morecraft KS, Gedney M, Ge J, Schroeder CM and van Hoesen GW.   2007.   Journal of Comparative Neurology, volume 500, pages 134-165.

(1729) Parallel thalamocortical pathways for echolocation and passive sound localization in a gleaning bat, Antrozous pallidus.   Razak KA, Shen W, Zumsteg T and Fuzessery ZM.   2007.   Journal of Comparative Neurology, volume 500, pages 322-358.

(1730) Adult neurogenesis: a common strategy across diverse species.   Sullivan JM, Benton JL, Sandeman DC and Beltz BS.   2007.   Journal of Comparative Neurology, volume 500, pages 574-584.

(1731) Right ventromedial prefrontal lesions result in paradoxical cardiovascular activation with emotional stimuli.   Hilz MJ, Devinsky O, Szczepanska H, Borod JC, Marthol H and Tutai M.   2006.   Brain, volume 129, pages 3343-3355.

(1732) Spatial and temporal dependencies of cross-orientation suppression in human vision.   Meese TS and Holmes DJ.   2007.   Proceedings. Biological Sciences / The Royal Society, volume 274, pages 127-136.

(1733) Conservation and evolution of gene coexpression networks in human and chimpanzee brains.   Oldham MC, Horvath S and Geschwind DH.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 17973-17978.

(1734) Germ-line epigenetic modification of the murine A vy allele by nutritional supplementation.   Cropley JE, Suter CM, Beckman KB and Martin DI.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 17308-17312.    Comment. Germ cells carry the epigenetic benefits of grandmother's diet.   Cooney CA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 17071-17072.

(1735) Evidence for different origin of sex chormosomes in snakes, birds, and mammals and step-wise differentiation of snake sex chromosomes.   Matsubara K, Tarui H, Toriba M, Yamada K, Nishida-Umehara C, Agata K and Matsuda Y.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 18190-18195.    Comment. Multiple independent origins of sex chromosomes in amniotes.   Vallender EJ and Lahn BT.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 1831-18032.

(1736) Testosterone increases bioavailability of carotenoids: insights into the honesty of sexual signaling.   Blas J, Perez-Rodriguez L, Bortolotti GR, Vinuela J and Marchant TA.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 18633-18637.

(1737) Relative blindsight in normal observers and the neural correlate of visual consciousness.   Lau HC and Passingham RE.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 18763-18768.

(1738) Sensory integration does not lead to sensory calibration.   Smeets JB, van den Dobbelsteen JJ, de Grave DD, van Beers RJ and Brenner E.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 18781-18786.

(1739) The development of siblings of children with autism at 4 and 14 months: social engagement, communication, and cognition.   Yirmiva N, Gamliel I, Pilowsky T, Feldman R, Baron-Cohen S and Sigman M.   2006.   Journal of Child Psychology and Psychiatry, and allied disciplines, volume 47, pages 511-523.

(1740) Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids.   Mirescu C, Peters JD, Noiman L and Gould E.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 19170-19175.

(1741) Almost all human genes resulted from ancient duplication.   Britten RJ.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 19027-19032.

(1742) A polymorphism in the norepinephrine transporter gene alters promoter activity and is associated with attention-deficit hyperactivity disorder.   Kim CH, Hahn MK, Joung Y, Anderson SL, Steele AH, Mazei-Robinson MS, Gizer I, Teicher MH, Cohen BM, Robertson D, Waldman ID, Blakely RD and Kim KS.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 19164-19169.

(1743) Time-dependent, layer-specific modulation of sensory responses mediated by neocortical layer 1.   Shlosberg D, Amitai Y and Azouz R.   2006.   Journal of Neurophysiology, volume 96, pages 3170-3182.

(1744) Identification of basolateral amygdala projection cells and interneurons using extracellular recordings.   Likhtik E, Pelletier JG, Popescu AT and Pare D.   2006.   Journal of Neurophysiology, volume 96, pages 3257-3265.

(1745) Language and the aging brain: patterns of neural compensation revealed by functional brain imaging.   Wingfield A and Grossman M.   2006.   Journal of Neurophysiology, volume 96, pages 2830-2839.

(1746) Chronic pain and the emotional brain: specific brain activity associated with spontaneous fluctuations of intensity of chronic back pain.   Baliki MN, Chialvo DR, Geha PY, Levy RM, Harden RN, Parrish TB and Apkarian AV.   2006.   Journal of Neuroscience, volume 26, pages 12165-12173.

(1747) Integration of new neurons into functional neural networks.   Ramirez-Amaya V, Marrone DF, Gage FH, Worley PF and Barnes CA.   2006.   Journal of Neuroscience, volume 26, pages 12237-12241.

(1748) Cross-modal processing in early visual and auditory cortices depends on expected statistical relationship of multisensory information.   Baier B, Kleinschmidt A and Muller NG.   2006.   Journal of Neuroscience, volume 26, pages 12260-12265.

(1749) The substantia nigra pars compacta and temporal processing.   Jahanshahi M, Jones CR, Dirnberger G and Frith CD.   2006.   Journal of Neuroscience, volume 26, pages 12266-12273.

(1750) Rethinking the fear circuit: the central nucleus of the amygdala is required for the acquisition, consolidation, and expression of Pavlovian fear conditioning.   Wilensky AE, Schafe GE, Kristensen MP and LeDoux JE.   2006.   Journal of Neuroscience, volume 26, pages 12387-12396.

(1751) Hippocampal sharp waves and reactivation during awake states depend on repeated sequential experience.   Jackson JC, Johnson A and Redish AD.   2006.   Journal of Neuroscience, volume 26, pages 12415-12426.

(1752) Monkey dorsolateral prefrontal cortex sends task-selective signals directly to the superior colliculus.   Johnston K and Everling S.   2006.   Journal of Neuroscience, volume 26, pages 12471-12478.

(1753) Distinct patterns of striatal medium spiny neuron activity during the natural sleep-wake cycle.   Mahon S, Vautrelle N, Pezard L, Slaght SJ, Deniau JM, Chouvet G and Charpier S.   2006.   Journal of Neuroscience, volume 26, pages 12587-12595.

(1754) Neural coding of tactile decisions in the human prefrontal cortex.   Pleger B, Ruff CC, Blankenburg F, Bestmann S, Wiech K, Stephan KE, Capilla A, Friston KJ and Dolan RJ.   2006.   Journal of Neuroscience, volume 26, pages 12596-12601.

(1755) Learning-induced plasticity in deep cerebellar nucleus.   Ohyama T, Nores WL, Medina JF, Riusech FA and Mauk MD.   2006.   Journal of Neuroscience, volume 26, pages 12656-12663.

(1756) Human taste thresholds are modulated by serotonin and noradrenaline.   Heath TP, Melichar JR, Nutt DJ and Donaldson LF.   2006.   Journal of Neuroscience, volume 26, pages 12664-12671.

(1757) Evidence of a nonlinear human magnetic sense.   Carrubba S, Frilot C 2nd, Chesson AL Jr and Marino AA.   2007.   Neuroscience, volume 144, pages 356-367.

(1758) Axonal site of spike initiation enhances auditory coincidence detection.   Kuba H, Ishii TM and Ohmori H.   2006.   Nature, volume 444, pages 1069-1072.

(1759) Intrasexual competition and sexual selection in cooperative mammals.   Clutton-Brock TH, Hodge SJ, Spong G, Russell AF, Jordan NR, Bennett NC, Sharpe LL and Manser MB.   2006.   Nature, volume 444, pages 1065-1068.   In the first sentence of the abstract, "...the sex that invests least in its offspring competes more intensely for access to the opposite sex...".

(1760) Group competition, reproductive leveling, and the evolution of human altruism.   Bowles S.   2006.   Science, volume 314, pages 1569-1572.

(1761) Ancient noncoding elements conserved in the human genome.   Venkatesh B, Kirkness EF, Loh YH, Halpern AL, Lee AP, Johnson J, Dandona N, Viswanathan LD, Tay A, Venter JC, Strausberg RL and Brenner S.   2006.   Science, volume 314, page 1892.

(1762) Characterizing a mammalian circannual pacemaker.   Lincoln GA, Clarke IJ, Hut RA and Hazlerigg DG.   2006.   Science, volume 314, pages 1941-1944.

(1763) Collateralization of the tectonigral projection with other major output pathways of superior colliculus in the rat.   Coizet V, Overton PG and Redgrave P.   2007.   Journal of Comparative Neurology, volume 500, pages 1034-1039.

(1764) Population size does not influence mitochondrial genetic diversity in animals.   Bazin E, Glemin S and Galtier N.   2006.   Science, volume 312, pages 570-572.

(1765) Motor responses of muscles supplied by cranial nerves to subthalamic nucleus deep brain stimuli.   Costa J, Valls-Sole J, Valldeoriola F, Rumia J and Tolosa E.   2007.   Brain, volume 130, pages 245-255.

(1766) Modafinil and unconstrained motor activity in schizophrenia. Double-blind crossover placebo-controlled trial.   Farrow TFD, Hunter MD, Haque R and Spence SA.   2006.   British Journal of Psychiatry, volume 189, pages 461-462.

(1767) Plasticity in animal personality traits: does prior experience alter the degree of boldness?   Frost AJ, Winrow-Giffen A, Ashley PJ and Sneddon LU.   2007.   Proceedings. Biological Sciences / The Royal Society, volume 274, pages 333-339.

(1768) Spread of arbitrary conventions among chimpanzees: a controlled experiment.   Bonnie KE, Horner V, Whiten A and de Waal FB.   2007.   Proceedings. Biological Sciences / The Royal Society, volume 274, pages 367-372.

(1769) Social personalities influence natal dispersal in a lizard.   Cote J and Clobert J.   2007.   Proceedings. Biological Sciences / The Royal Society, volume 274, pages 383-390.

(1770) Impairments in frontal cortical {gamma} synchrony and cognitive control in schizophrenia.   Cho RY, Konecky RO and Carter CS.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 19878-19883.

(1771) The discordant ear drum.   Fay JP, Puria S and Steele CR.   2006.   Proceedings of the National Academy of Sciences of the United States of America, volume 103, pages 19743-19748.

(1772) NMDA-dependent facilitation of corticostriatal plasticity by the amygdala.   Popescu AT, Saghyan AA and Pare D.   2007.   Proceedings of the National Academy of Sciences of the United States of America, volume 104, pages 341-346.

(1773) How personal experience modulates the neural circuitry of memories of September 11.   Sharot T, Martorella EA, Delgado MR and Phelps EA.   2007.   Proceedings of the National Academy of Sciences of the United States of America, volume 104, pages 389-394.

(1774) Positive affect increases the breadth of attentional selection.   Rowe G, Hirsh JB and Anderson AK.   2007.   Proceedings of the National Academy of Sciences of the United States of America, volume 104, pages 383-388.

(1775) Sequential structure of neocortical spontaneous activity in vivo.   Luczak A, Bartho P, Marquet SL, Buzsaki G and Harris KD.   2007.   Proceedings of the National Academy of Sciences of the United States of America, volume 104, pages 347-352.

(1776) Penetrating arterioles are a bottleneck in the perfusion of neocortex.   Nishimura N, Schaffer CB, Friedman B, Lyden PD and Kleinfeld D.   2007.   Proceedings of the National Academy of Sciences of the United States of America, volume 104, pages 365-370.

(1777) A neural basis for inference in perceptual ambiguity.   Sterzer P and Kleinschmidt A.   2007.   Proceedings of the National Academy of Sciences of the United States of America, volume 104, pages 323-328.

(1778) Neural substrates of envisioning the future.   Szpunar KK, Watson JM and McDermott KB.   2007.   Proceedings of the National Academy of Sciences of the United States of America, volume 104, pages 642-647.

(1779) Evolutionary changes in cis and trans gene regulation.   Wittkopp PJ, Haerum BK and Clark AG.   2004.   Nature, volume 430, pages 85-88.   In this study, trans-regulatory differences were inferred, and were always accompanied by cis-regulatory changes. So, did trans-regulatory differences exist in the terms of this study? Do trans-regulatory differences exist in the terms of this study? The prefixes trans- and cis- were used originally to describe a relationship with the Alps, so how can they be expected to characterise genetic complexity? Would the prefixes trans- and cis- withstand an inter-rater reliability study? Better to say changes within chromosome pairs, and changes between chromosome pairs, and then number the chromosomes, according to the simple rules of numerical language.

(1780) Plasticity compartments in basal dendrites of neocortical pyramidal neurons.   Gordon U, Polsky A and Schiller J.   2006.   Journal of Neuroscience, volume 26, pages 12717-12726.

(1781) A physiologically plausible model of action selection and oscillatory activity in the basal ganglia.   Humphries MD, Stewart RD and Gurney KN.   2006.   Journal of Neuroscience, volume 26, pages 12921-12942.

(1782) Regional