Neuropsychiatry Disorders Research Articles

Molecular biology research in neuropsychiatry: India′s contribution

Neuropsychiatric disorders represent the second largest cause of morbidity worldwide. These disorders have complex etiology and patho-physiology. The major lacunae in the biology of the psychiatric disorders include genomics, biomarkers and drug discovery, for the early detection of the disease, and have great application in the clinical management of disease. Indian psychiatrists and scientists played a significant role in filling the gaps. The present annotation provides in depth information related to research contributions on the molecular biology research in neuropsychiatric disorders in India. There is a great need for further research in this direction as to understand the genetic association of the neuropsychiatric disorders; molecular biology has a tremendous role to play. The alterations in gene expression are implicated in the pathogenesis of several neuropsychiatric disorders, including drug addiction and depression. The development of transgenic neuropsychiatric animal models is of great thrust areas. No studies from India in this direction. Biomarkers in neuropsychiatric disorders are of great help to the clinicians for the early diagnosis of the disorders. The studies related to gene-environment interactions, DNA instability, oxidative stress are less studied in neuropsychiatric disorders and making efforts in this direction will lead to pioneers in these areas of research in India. In conclusion, we provided an insight for future research direction in molecular understanding of neuropsychiatry disorders.

Blockade of [11C](+)-PHNO binding in human subjects by the dopamine D3 receptor antagonist ABT-925

Dopamine D3 receptors are preferentially localized in the limbic system and midbrain, and thus may be involved in the pathophysiology of neuropsychiatry disorders. [11C](+)-PHNO is the first preferential D3 receptor radioligand in humans, yet there are no blockade studies with a D3 receptor antagonist in humans. This study characterized the blockade of [11C](+)-PHNO binding by ABT-925, a D3 receptor antagonist, in healthy male subjects. Sixteen subjects underwent 2-3 positron emission tomography (PET) scans, at baseline and following one or two doses of ABT-925 ranging from 50 mg to 600 mg. Receptor occupancies were estimated for globus pallidus, substantia nigra, caudate, putamen, and ventral striatum. At the 600-mg dose (n=9), ABT-925 receptor occupancy (mean+/-s.d.) was higher in substantia nigra (75+/-10%) and globus pallidus (64+/-22%) than in ventral striatum (44+/-17%), caudate (40+/-18%) and putamen (38+/-17%) (ANOVA: F4,140=15.02, p<0.001). The fractions of [11C](+)-PHNO binding attributable to D3 receptors in D3 receptor-rich regions were 100% (substantia nigra) and 90% (globus pallidus), and in D2 receptor-rich regions were 55% (caudate) and 53% (putamen). The ED50 of ABT-925 was 4.37 microg/ml across regions. Our results demonstrate that [11C](+)-PHNO binding can be blocked by a D3 receptor antagonist and confirm preclinical findings that [11C](+)-PHNO signal in the substantia nigra and globus pallidus is mainly reflective of its binding to D3 receptors. Thus, [11C](+)-PHNO seems a suitable PET radiotracer to estimate D3 receptor occupancy in humans.

Dopamine D3 Receptor Antagonist SB-277011A Influences Cell Firing in the Rat Ventral Tegmental Area, Parallel Role with the Cannabinoid System in Addiction and Neuropsychiatry Disorders?

SB-277011A is a compound entering the brain with high affinity and selectivity for the dopamine (DA) D3 receptor. Recent electrophysiological study has shown that acute oral administration of SB-277011A significantly alters the spontaneous activity of DA neurons in the ventral tegmental area (VTA) but that intravenous administration has no effects. In that electrophysiological study hypotheses to explain this discrepancy involved either administration route- dependent timing for the compound to reach its active site or the formation of an active metabolite following oral administration that would sustain the activity of SB-277011A on DA cell firing. In an attempt to assess whether formation of a metabolite may account for the activity of the parent compound we conducted electrophysiological multi-unit field recordings of DA neurons in the VTA of anaesthetised rats following treatment with SB-277011A either systemically or locally in the VTA. The local dose (2.5� g) was selected based on brain exposure achieved following systemic i.p. administration of 10mg/kg. Results show that both administrations increased VTA neurons firing compared to vehicle administration. However, local injection of SB-277011A in the VTA induced a more rapid and higher increase of neuronal activity than systemic treatment. These results suggest that the increased VTA cell firing occurring following systemic administration of SB-277011A is likely due to the compound itself and not to a putative metabolite. Finally, since the growing evidence that cannabinoids (CBs) modulate DA release in the brain and in view of the fact that CB1 receptors are widely distributed over DA neurons, the interplay between these two systems in the context of the current findings is discussed.

Effects of sex hormonal levels and phases of the menstrual cycle in the processing of emotional faces

Several neuropsychiatry disorders have shown a sexual dimorphism in their incidence, symptom profile and therapeutic response. A better understanding of the impact of sex hormones in emotional processing sexual dimorphism could bring light to this important clinical finding. Some studies have provided evidence of sex differences in the identification of emotional faces, however, results are inconsistent and such inconsistency could be related to the lack of experimental control of the sex hormone status of participants. More recently, a few studies evaluated the modulation of facial emotion recognition by the phase of the menstrual cycle and sex hormones, however, none of them directly compared these results with a group of men. We evaluated the accuracy of facial emotion recognition in 40 healthy volunteers. Eleven women were assigned to early follicular group, nine women to the ovulatory group and 10 women to luteal group, depending on the phase of menstrual cycle, and a group of 10 men were also evaluated. Estrogen, progesterone and testosterone levels were assessed. The performance of the groups in the identification of emotional faces varied depending on the emotion. Early follicular group were more accurate to perceive angry faces than all other groups. Sadness was more accurately recognized by early follicular group than by luteal group and regarding the recognition of fearful faces a trend to a better performance and a significantly higher accuracy was observed, respectively, in the early follicular group and in the ovulatory group, in comparison to men. In women, estrogen negatively correlated to the accuracy in perception of angry male faces. Our results indicate sex hormones to be implicated in a sexual dimorphism in facial emotion recognition, and highlight the importance of estrogen specifically in the recognition of negative emotions such as sadness, anger and fear.

BOOKS

Acta Neurologica ScandinavicaVolume 64, Issue 4 p. 301-302 BOOKS First published: October 1981 https://doi.org/10.1111/j.1600-0404.1981.tb04409.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Abstract M. R. Trimble: Neuropsychiatry Disorders of movement. Ed. by A. Barbeau Neuroreceptors - basic and clinical aspects. Ed. by E. Usdin, W. Bunney, Jr. & J. M. Davis Volume64, Issue4October 1981Pages 301-302 RelatedInformation

The leukocytes expressing DARPP-32 are reduced in patients with schizophrenia and bipolar disorder

Bipolar disorder (BPD) and schizophrenia (SCZ) are severe disorders representing an enormous social, familiar and individual burden, being SCZ the most disabling psychiatric disorder characterized by psychosis and cognitive impairment. It is well known that SCZ and BPD are associated with abnormalities in dopamine signaling pathway. Recent data in the literature have demonstrated altered expression levels of some proteins involved in the modulation of this pathway in both brain and peripheral tissues. It was shown that protein and mRNA levels of dopamine and cAMP regulated phosphoprotein (DARPP-32) were downregulated in dorsolateral prefrontal cortex (DLPFC) of patients with SCZ or BPD when compared to controls. Due to the difficulty to access brain tissue and the absence of objective laboratory tests for bio-markers, we measured DARPP-32 expression in blood cell sub-populations (CD4+ T lymphocytes, CD56+ NK cells, CD19+ B lymphocytes and CD14+ monocytes) taking advantage of the close relation of nervous and immune systems. Using flow cytometry as the analytical method, our results have shown that the DARPP-32 expression was diminished in CD4+ T lymphocytes, CD19+ B lymphocytes and CD14+ monocytes of BPD patients and was also decreased in CD4+ T lymphocytes and CD56+ NK cells of SCZ patients. These results showed that DARPP-32 expression in immune cells agrees with reports of reduced DARPP-32 protein in the DLPFC of BPD or SCZ patients. Our data suggest that DARPP-32 expression in PBMC could be used as a source of bio-markers to help in the treatment response of neuropsychiatry disorders as a window to the changes in the brain of those patients.

Williams Syndrome: A Genetic Deletion Disorder Presenting Clues to the Biology of Sociability and Clinical Challenges of Hypersociability

Williams syndrome is a neurodevelopmental disorder that results from the deletion of approximately 25-30 genes spanning about 1.5 megabases in the q11.23 region of chromosome 7. Patients with this syndrome present with a combination of a distinctive elfin-like facial appearance; growth retardation; mild mental retardation; an inconsistent cognitive profile that includes visuospatial impairments with good facial discrimination and relatively preserved expressive language skills; and cardiovascular abnormalities. In addition, a striking behavioral feature of the syndrome is the high sociability and empathy that these patients show for others. The study of patients with "partial" deletions of the chromosome band 7q11.23, mutated genes in this region and knockout mice with deletions of specific genes in the homologous G1-G2 region of mouse chromosome 5 are clarifying some genotype/phenotype relationships. Furthermore, genes located in this region that are prominently expressed have been implicated in brain development and function. The neuropsychological profile of patients with Williams syndrome is heterogeneous, highlights important dissociations between cognitive functions and suggests that the behavioral dimensions of sociability, empathy, engageability, and talkativeness may be independent of, or not easily explained by, the cognitive deficits. Williams syndrome has enormous heuristic value because its pathological feature of heightened "sociability" can be a "deficit" symptom of major complex neuropsychiatric disorders, such as schizophrenia and autism. Data consistent with a core inability of patients with Williams syndrome to inhibit social approach suggest that this disorder may afford an opportunity to study the biological basis of the "drive" toward socialization. From a research perspective, the syndrome lends itself to neurobiological studies of sociability as a dimension that varies independently of cognition (or at least many separable cognitive processes). Importantly, from a clinical perspective, the syndrome challenges us to administer strategic psychosocial interventions that take advantage of the opportunities that "pathological" sociability provide, while avoiding its threats. An illustrative example of an effective strategically planned psychosocial intervention for a patient with Williams syndrome is briefly presented.

Eating Disorder Paradigms for the New Millennium: Do “Attachment” and “Culture” Appear on Brain and Genome Scans?

Arguably, eating disorders have inspired more shifts in explanatory paradigms, over a shorter span of time, than have any other class of syndromes in the history of psychiatry. We once understood anorexia nervosa (AN) to be a response to well-meaning but overbearing intrusions of anxious parents (usually mothers) that drove affected children into a compensatory stance of food refusal-presumably, the sole means of self-assertion left to these unfortunate children. This construal was tempting, partly because the parents of children with AN all seemed to be so anxious and partly because daughters with AN all seemed to be so obstinate and oppositional. However, careful attention to family interaction and attachment patterns showed that the parents in question were often anxious for no other reason than that watching one's child starve herself provokes anxiety. These anxious parents often enough failed to accommodate their daughters' simultaneous calls for protection, validation, and autonomy.' Likewise, we understood bulimia nervosa (BN) to be a misguided protest against parental dysempathy, hostility, and indeed sometimes, cruelty-a desperate grappling on the part of developmentally damaged children to gratify need through unbridled bingeing and then reject what was obtained through purging.2 These metaphors had emotional appeal but did not have sufficiently universal application. There followed the era of defining eating disorders as culture-bound syndromes or social epidemics.3 Clearly, cultural messages about the importance of dieting and slimness have a lot to do with eating disorders. However, emerging cross-cultural and historical data began to reveal a startling truth: eating disorders, especially AN, have occurred throughout the history of civilized societies, and indeed, in societies not even brushed by pressures to be thin. AN, at least, began to look less like a socioculturel creation and more like a hereditary syndrome akin to such entities as schizophrenia or bipolar disorder.4 Indicating a swing to yet another etiologic concept, prototypic opening phrases in articles from the late 1990s often read something like the following: Once thought to embody a cultural preoccupation with dieting, AN and BN have come to be increasingly defined as neuropsychiatrie disorders with strong genetic determinants. This shift in perspective has reflected some central additions during the past 10 to 15 years to the knowledge base on eating disorders. Family epidemiologic and twin data have shown that the eating disorders are heritable, whereas neurobiological, genetic association, and linkage studies have provided clues as to what factors might transmit vulnerability.5-7 Important changes in weightings assigned to psychological-developmental and neurobiological-genetic factors have clearly been in order. Another competition among concepts has also unfolded as an undercurrent, relating to the question of whether to view the eating disorders as disturbances of self-, mood, and impulse regulation or as disturbances of mechanisms governing appetite and weight control. In other words, are eating disorders feeding disorders, or are they variants of anxiety, mood, and impulse control disorders? Proponents of the first view search for causes among agents known to influence eating behaviour directly (such as leptin, ghrelin, and brain-derived neurotrophic factor) and among neurotransmitters that regulate satiety and reward from food (such as serotonin and dopamine).8 Advocates of the second perspective emphasize the ways in which the eating disorders resemble mood, anxiety, and impulse control disorders and construe eating symptoms as secondary or epiphenomenological aspects of phobic food avoidance. The problem is that exponents of the feeding disorder model sputter when asked to explain why eating disorders coincide so frequently with other psychiatric problems (such as affective or personality disorders), whereas adherents of the second camp never give a satisfying answer a deceptively simple question: Why is it an eating disorder? …

Consultation liaison psychiatry in Norway

The history of Norwegian CL psychiatry dates back to 1951 when a psychiatrist was appointed to perform psychiatric consultations at the National Hospital. Over the next 20 years, two more psychiatrists were appointed at the same hospital. A separate department was established in 1972 and is now known as the Department of Psychosomatic Medicine, which is under the leadership of Professor Ulrik F. Malt. The department has been steadily growing, mainly after the head of the department also became professor at the University of Oslo in 1985. In the beginning, the department had only psychiatrists, now, there are 9 medical doctors and 6 psychologists, as well as nurses, physiotherapists, and secretaries, for a total of 24 staff members. The department is the leading CL unit in Norway, with regard to magnitude and broadness of clinical and scientific activities. In addition to meeting hospital requirements, it employs several general practitioners and specialists. It is the only Norwegian CL unit with an outpatient clinic. In addition to general CL services to patients with various medical disorders, special services are given within the field of complex psychosomatic or affective disorders, clinical psychopharmacology, neuropsychiatry, and gender identity disorder. At Ulleval University Hospital, which is the Norwegian hospital with the most number of beds, a part-time psychiatrist was affiliated to one of the medical departments in the late 1950s, mainly working with patients with lung disease and, later, with those with cardiac problems. In the late 1970s, a full-time CL psychiatrist was appointed. The psychiatric department had no formal CL unit, and the psychiatrists on duty, often young residents, provided the service. The author has been working as a consultant psychiatrist at the Department of Acute Medicine since

Diagnoses and Antipsychotic Treatment Among Youths in a Public Mental Health System

The use of antipsychotics, namely newer atypical agents, has increased significantly in children and adolescents. It is important to examine diagnoses associated with antipsychotic treatment in youths. To evaluate trends in psychiatric diagnoses of children and adolescents in a public mental health system who were prescribed antipsychotics. Children and adolescents, up to the age of 19 years, who were prescribed an antipsychotic between January 1998 and December 2001 were identified using the Texas Medicaid Vendor Drug database. Patient identification numbers were then cross-linked to the Client Assignment and Registration database of the Texas Department of Mental Health and Mental Retardation to extract diagnostic data. Disruptive behavioral disorders accounted for the highest percentage (35%) of diagnoses associated with children and adolescents receiving antipsychotic treatment and mental healthcare services. Depressive disorders were the second most common diagnosis (18%), and bipolar disorders accounted for roughly 12% of all diagnoses. Approximately 3% of children and adolescents did not have a psychiatric diagnosis. The percentage of youths with comorbid psychiatric diagnoses decreased over time. Although disruptive behavioral disorders accounted for a large percentage of antipsychotic use in this population, these findings suggest that antipsychotics are being used to treat other psychiatric diagnoses, for which limited supporting data exist. Future research in children and adolescents should aim to provide needed efficacy and safety data of antipsychotics across the spectrum of neuropsychiatric disorders.

Effects of acute amphetamine in the mediodorsal nucleus of the thalamus: possible relevance for psychiatric disorders Amphetamine administration alters thalamic activity

Disruptions in the thalamocortical circuit have been related to several psychiatric disorders, such as schizophrenia and obsessive-compulsive disorders. The dopaminergic/GABAergic afferents to the limbic thalamocortical circuit originate in the ventral tegmental area (VTA) and play a crucial role in the regulation of the normal cognitive functions mediated by this circuit. Moreover, it has been shown that the dopaminergic modulatory system is altered in schizophrenics. Despite the strong clinical and behavioral evidence of the importance of the thalamocortical circuit and the mesocortical dopamine (DA) system for normal cognitive function, little is known about the basic synaptic interactions between the thalamus and VTA. This research hypothesized that VTA stimulation would evoke DAergic and/or GABAergic-mediated responses in the MD thalamic neurons. Using intracellular recordings in vivo, it was found that VTA stimulation evoked short latency EPSPs in 73% of the recorded MD neurons and IPSPs-like responses in 16% of the MD cells. The nature of the VTA-MD projection was explored using DAergic and GABAergic drugs. It was found that the indirect DAergic agonist amphetamine affects the spontaneous and VTA-mediated responses recorded in the MD thalamus. These results indicate that the VTA projection contributes to the modulation of MD activity and that the disruption of such modulation may be relevant in neuropsychiatry disorders.

Effects of acute amphetamine in the mediodorsal nucleus of the thalamus: possible relevance for psychiatric disorders: Amphetamine administration alters thalamic activity

Disruptions in the thalamocortical circuit have been related to several psychiatric disorders, such as schizophrenia and obsessive-compulsive disorders. The dopaminergic/GABAergic afferents to the limbic thalamocortical circuit originate in the ventral tegmental area (VTA) and play a crucial role in the regulation of the normal cognitive functions mediated by this circuit. Moreover, it has been shown that the dopaminergic modulatory system is altered in schizophrenics. Despite the strong clinical and behavioral evidence of the importance of the thalamocortical circuit and the mesocortical dopamine (DA) system for normal cognitive function, little is known about the basic synaptic interactions between the thalamus and VTA. This research hypothesized that VTA stimulation would evoke DAergic and/or GABAergic-mediated responses in the MD thalamic neurons. Using intracellular recordings in vivo, it was found that VTA stimulation evoked short latency EPSPs in 73% of the recorded MD neurons and IPSPs-like responses in 16% of the MD cells. The nature of the VTA-MD projection was explored using DAergic and GABAergic drugs. It was found that the indirect DAergic agonist amphetamine affects the spontaneous and VTA-mediated responses recorded in the MD thalamus. These results indicate that the VTA projection contributes to the modulation of MD activity and that the disruption of such modulation may be relevant in neuropsychiatry disorders.

Brain aging research at the close of the 20th century: from bench to bedside

Remarkable and continued growth in the field of brain aging research has been fueled by a confluence of factors. Developments in molecular biology, imaging, and genetics coupled with the imperative caused by the aging of the population has created fertile ground for improved understanding of the interaction between brain function and behavior. Aging changes in neurochemical systems may account for the spectrum of cognitive and behavioral states of successfully aged pen sons, but may also contribute to enhanced vulnerability to depressive or dementing illness. In particular, the refinement of in vivo imaging approaches to investigating the structure and function of the aging brain has provided the opportunity to strengthen our knowledge of the biological substrate of the aging brain and neuropsychiatrie disorders, and translate these into therapeutics.

MSHAKE. A tool for measuring staff knowledge related to geriatric mental health.

This article describes the development of a knowledge-screening instrument used with staff caring for elderly patients with neuropsychiatric disability. A 25-item tool, referred to as the Mary Starke Harper Aging Knowledge Exam (MSHAKE), was developed to verify knowledge competencies of 171 employees at a geropsychiatric center in the Southeastern United States. The MSHAKE assesses basic geriatric mental health knowledge in an educationally diverse health care work force. A variety of descriptive and inferential statistics provide preliminary evidence supporting the use of the MSHAKE as an effective measure of staff members' essential knowledge of aging and neuropsychiatric disorders. This tool has practical application in the clinical setting as part of a competency verification system or in-service evaluation.

Season of birth in suicidology: Neurobiological and epidemiological studies

Background: Several neuropsychiatrie disorders have shown season of birth associations. Low cerebrospinal fluid (CSF) levels of the serotonin metabolite 5-HIAA and the dopamine metabolite HVA have ...

Book reviews

Book reviewed in this article:Neurodevelopment and Adult Psychopathology Edited by Matcheri S Keshaven, Robin M MurrayNeuroimaging in Child Neuropsychiatry Disorders Edited by B GarreauMedical Aspects of Developmental Disabilities in Children Birth to Three, Third Edition Edited by James A BlackmanMosby's Resource Guide to Children with Disabilities and Chronic Illness Edited by Helen M Wallace, John C MacQueen, Robert F Biehl, James A Blackman

Sexual dimorphism of the developing human brain

1. 1. Sexual dimorphism of human brain anatomy has not been well-studied between 4 and 18 years of age, a time of emerging sex differences in behavior and the sexually specific hormonal changes of adrenarche (the predominantly androgenic augmentation of adrenal cortex function occurring at approximately age 8) and puberty. 2. 2. To assess sex differences in brain structures during this developmental period volumes of the cerebrum, lateral ventricles, caudate, putamen, globus pallidus temporal lobe, amygdala, and hippocampus, and midsagittal area measurements of the corpus callosum were quantified from brain magnetic resonance images of 121 healthy children and adolescent and examined in relation to age and sex. 3. 3. Males had a 9% larger cerebral volume. When adjusted for cerebral volume by ANCOVA only the basal ganglia demonstrated sex differences in mean volume with the caudate being relatively larger in females and the globus pallidus being relatively larger in males. The lateral ventricles demonstrated a prominent sex difference in brain maturation with robust increases in size in males only. A piecewise-linear model revealed a significant change in the linear regression slope of lateral ventricular volume in males after age 11 that was not shared by females at that or other ages. 4. 4. Amygdala and hippocampal volume increased for both sexes but with the amygdala increasing significantly more in males than females and hippocampal volume increasing more in females. 5. 5. These sexually dimorphic patterns of brain development may be related to the observed sex differences in age of onset, prevalence, and symptomatology seen in nearly all neuropsychiatrie disorders of childhood.

The distribution of tyrosine hydroxylase-immunoreactive fibers in the human entorhinal cortex

The entorhinal cortex plays an important role in learning and memory, and it has been implicated as a site of dysfunction in some neuropsychiatric disorders such as schizophrenia. The organization of many components of the neural circuitry of this region, including dopaminergic afferents, has not been studied in detail. Using immunohistochemical techniques, we examined the density and laminar distribution of axons immunoreactive for tyrosine hydroxylase, the rate limiting enzyme in catecholamine biosynthesis, in the entorhinal cortex of eight control human brains. The density of tyrosine hydroxylase-containing axons decreased from rostral to caudal regions of entorhinal cortex. In addition, there was a prominent medial to lateral gradient of increasing fiber density. This gradient extended into the adjacent transentorhinal cortex, which contained the highest density of labeled axons of the regions studied. The laminar distribution of tyrosine hydroxylase-containing fibers also differed among the subdivisions of the entorhinal cortex. A bilaminar pattern of labeled axons in layers deep I-superficial II and in deep layer VI was present in the intermediate and caudal subdivisions of entorhinal cortex. In contrast, the olfactory and rostral subdivisions, as well as portions of the transentorhinal region, contained a trilaminar pattern, with a high density of tyrosine hydroxylase-immunoreactive axons in layers deep I-superficial II, deep III–IV and deep VI. In addition, radially-oriented bands of labeled fibers were observed extending between deep layer I and layer III, particularly in the rostral subdivision of the entorhinal cortex. In summary, tyrosine hydroxylase-containing afferents to the human entorhinal cortex are distributed in a characteristic regional and laminar pattern, and the lateral regions of the entorhinal cortex and the adjacent transentorhinal cortex are particularly densely innervated. These data contribute to the understanding of the normal circuitry of the human entorhinal cortex, and are of potential relevance to the pathophysiology of certain neuropsychiatrie disorders, such as schizophrenia.

Psychiatric contributions to the undergraduate medical curriculum

Within medicine, psychiatry is seen as a specialist subject, especially insofar as it deals with psychosis and other severe mental illness. Accordingly, it is often taught in medical schools alongside other so-called specialist subjects such as paediatrics and obstetrics and gynaecology. These are seen to contrast to generalist subjects such as medicine and surgery, but which them selves are usually taught within the framework of highly specialised firms concentrating on one or two organs or systems within the body. Within psychiatry there are specialist areas of practice. Some of these are recognised formally by our College and by the health service, e.g. child and adolescent psychiatry, psychiatry of addictive behaviour, psychiatry of learning dis ability, and forensic psychiatry. Others are less generally recognised and are more likely to be the consequence of idiosyncratic service or research developments, e.g. disorders of eating, sleeping and sexual function, neuropsychiatry, and puerperal disorders. This applies also to certain treatment approaches. For instance, milieu therapy and behavioural psychotherapy are less universally developed in psychiatric practice within the health service than is dynamic psychotherapy. Paradoxically it is some such categories of highly specialist practice which reflect more commonplace disorders within the general population. Psychiatric teaching to undergraduates often focuses on the major illnesses and their treat ment and management. All students clearly need to know how to identify the major psychoses and to know, in broad terms, about their long-term management, both in respect of compliance problems, and the importance of teamwork, management skills and working in the com munity alongside primary care systems. Psy chiatry provides a most useful and potentially well structured opportunity for medical students to experience working in the community. Medical students also especially need to know in a thorough way about the protean expressions of depression and how to assess suicide risk. However, other subject areas are equally impor tant for the medical student, and psychiatry is often turned to as a discipline that might be able to contribute to and take the lead in such teaching. One such area which psychiatrists themselves have a variety of views about their competence to spearhead in this way is 'communication skills'.

Immunocytochemical localization and description of neurons expressing serotonin 2 receptors in the rat brain

Serotonin 2 receptors have been implicated in a variety of behavioral and physiological processes, as well as a number of neuropsychiatrie disorders. To specify the brain regions and specific cell types possessing serotonin 2 receptors, we conducted an immunocytochemical study of the rat brain using a polyclonal serotonin 2 receptor antibody. Perfusion-fixed rat brain sections were processed for immunocytochemistry and reactivity was visualized using an immunoperoxidase reaction. Numerous small, round neurons were heavily labeled in the granular and periglomerular regions of the olfactory bulb. Heavy labeling of medium-sized multipolar and bipolar neurons was also seen in olfactory regions of the ventral forebrain, including the anterior olfactory nucleus and olfactory tubercle. Other regions of the basal forebrain exhibiting high levels of immunoreactivity were the nucleus accumbens, ventral pallidum, Islands of Calleja, fundus striatum and endopyriform nucleus. Immunoreactive neurons were also seen in the lateral amygdala. A dense band of small, round cells was stained in layer 2 of pyriform cortex. In neocortex, a very sparse and even distribution of bipolar and multipolar neurons was seen throughout layers II–VI. A much more faintly labeled population of oval cells was observed in the deep layer of retrosplenial and posterior cingulate cortex, and in the granular layer of somatosensory frontoparietal cortex. A moderate number of medium bipolar and multipolar cells were scattered throughout the neostriatum, and a moderate number of pyramidal and pyramidal-like cells were seen in the CA fields of the hippocampus. Diencephalic areas showing immunolabeling included the medial habenula and anterior pretectal nucleus, with less labeling in the ventral lateral geniculate. In the hindbrain, two dense populations of large multipolar cells were heavily labeled in the pedunculopontine and laterodorsal tegmental nuclei, with lesser labeling in the periaqueductal gray, superior colliculus, spinal trigeminal nucleus and nucleus of the solitary tract. Based on the distribution, localization and morphology of immunoreactive neurons in these regions, we hypothesize that subpopulations of serotonin 2 containing cells may be GABAergic interneurons or cholinergic neurons. Further, the observed distribution suggests that the physiological effects of serotonin acting through serotonin 2 receptors are mediated by a relatively small number of cells in the brain. These observations may have strong functional implications for the pharmacological treatment of certain neuropsychiatrie disorders.