Attitudes toward neuroscience education in psychiatry: a national multi-stakeholder survey.

OBJECTIVE: The objective of this study is to assess the attitudes of chairs of psychiatry departments, psychiatrists, and psychiatry trainees toward neuroscience education in residency programs and beyond in order to inform future neuroscience education approaches. METHOD: This multi-stakeholder survey captured data on demographics, self-assessments of neuroscience knowledge, attitudes toward neuroscience education, preferences in learning modalities, and interests in specific neuroscience topics. In 2012, the authors distributed the surveys: by paper to 133 US psychiatry department chairs and electronically through the American Psychiatric Association to 3,563 of its members (1,000 psychiatrists and 2,563 trainees). RESULTS: The response rates for the chair, psychiatrist, and trainee surveys were 53, 9, and 18 %, respectively. A large majority of respondents agreed with the need for more neuroscience education in general and with respect to their own training. Most respondents believed that neuroscience will help destigmatize mental illness and begin producing new treatments or personalized medicines in 5-10 years. Only a small proportion of trainees and psychiatrists, however, reported a strong knowledge base in neuroscience. Respondents also reported broad enthusiasm for transdiagnostic topics in neuroscience (such as emotion regulation and attention/cognition) and description at the level of neural circuits. CONCLUSIONS: This study demonstrates the opportunity and enthusiasm for teaching more neuroscience in psychiatry among a broad range of stakeholder groups. A high level of interest was also found for transdiagnostic topics and approaches. We suggest that a transdiagnostic framework may be an effective way to deliver neuroscience education to the psychiatric community and illustrate this through a case example, drawing the similarity between this neuroscience approach and problem-based formulations familiar to clinicians.

Attitudes toward neuroscience education among psychiatry residents and fellows.

OBJECTIVE: The purpose of this study is to assess the attitudes of psychiatry trainees toward neuroscience education in psychiatry residency and subsequent training in order to inform neuroscience education approaches in the future. METHODS: This online survey was designed to capture demographic information, self-assessed neuroscience knowledge, attitudes toward neuroscience education, preferences in learning modalities, and interest in specific neuroscience topics. Volunteers were identified through the American Psychiatric Association, which invited 2,563 psychiatry trainees among their members. RESULTS: Four hundred thirty-six trainees completed the survey. Nearly all agreed that there is a need for more neuroscience education in psychiatry residency training (94%) and that neuroscience education could help destigmatize mental illness (91%). Nearly all (94%) expressed interest in attending a 3-day course on neuroscience. Many neuroscience topics and modes of learning were viewed favorably by participants. Residents in their first 2 years of training expressed attitudes similar to those of more advanced residents and fellows. Some differences were found based on the level of interest in a future academic role. CONCLUSIONS: This web-based study demonstrates that psychiatry residents see neuroscience education as important in their training and worthy of greater attention. Our results suggest potential opportunities for advancing neuroscience education.

Bringing Neuroscience to the Bedside.

Clinical psychiatry has not historically expected practitioners to learn the basic science of psychiatric illness. Despite wide recognition that all effective psychiatric treatments have neurophysiological mechanisms, the field has struggled to integrate concepts of the mind and brain. Because of historical separations of clinical psychiatry and evolving neuroscience research, many psychiatric residency programs feel underresourced to teach clinically relevant neuroscience, and current residency graduates are not being prepared to integrate neuroscience findings into their practice. Significant strides have been made in the understanding of the neurobiology of psychiatric disorders. Similarly, the neurobiological mechanisms of a wide variety of treatments have been elucidated, spanning interventions from psychotherapy to physical exercise, electroconvulsive therapy, and modern neuromodulation techniques. The authors discuss strategies for integrating the language of clinical neuroscience into everyday psychiatric practice and review resources available to clinicians and trainees to help them acquire and practice these skills.

Metabotropic glutamate receptor 2 and 3 gene expression in the human prefrontal cortex and mesencephalon in schizophrenia.

Group II metabotropic glutamate receptors (mGluR2 and mGluR3) are implicated in schizophrenia. We characterized mGluR2 and 3 mRNA in the human prefrontal cortex (PFC) and mesencephalon, and then compared cases with schizophrenia to matched controls. In the human brain, both receptors were expressed in the PFC and, unlike the rodent, in dopaminergic (DA) cell groups. In schizophrenia, we found significantly higher levels of mGluR2 mRNA in the PFC white matter. The expression of mGluR2, 3 in DA cells provide a mechanism for glutamate to modulate dopamine release in the human brain and this species-specific difference may be critical to understanding rodent models in schizophrenia.

Catechol-O-methyltransferase genotype and dopamine regulation in the human brain.

A functional polymorphism in the gene for catechol-O-methyltransferase (COMT) has been shown to affect executive cognition and the physiology of the prefrontal cortex in humans, probably by affecting prefrontal dopamine signaling. The COMT valine allele, associated with relatively poor prefrontal function, is also a gene that may increase risk for schizophrenia. Although poor performance on executive cognitive tasks and abnormal prefrontal function are characteristics of schizophrenia, so is psychosis, which has been related to excessive presynaptic dopamine activity in the striatum. Studies in animals have shown that diminished prefrontal dopamine neurotransmission leads to upregulation of striatal dopamine activity. We measured tyrosine hydroxylase (TH) mRNA in mesencephalic dopamine neurons in human brain and found that the COMT valine allele is also associated with increased TH gene expression, especially in neuronal populations that project to the striatum. This indicates that COMT genotype is a heritable aspect of dopamine regulation and it further explicates the mechanism by which the COMT valine allele increases susceptibility for psychosis.

Reliability of psychiatric diagnosis in postmortem research.

BACKGROUND: Postmortem human brain research is an important approach for identifying the cellular, molecular, and genetic pathways involved in the pathophysiology of psychiatric disorders. One critical component in postmortem research is the reliability of psychiatric diagnoses used to define study cohorts. Finding reliable methods for assessing lifetime psychiatric diagnoses in subjects after death is extremely challenging. METHODS: Two commonly used approaches were compared: psychiatric record reviews and postmortem family interviews. We hypothesized that these two methods would lead to more diagnostic agreement for subjects with schizophrenia than those with mood disorders. For 37 cases, psychiatric records were reviewed retrospectively using the Diagnostic Evaluation After Death, and family members were interviewed using the Structured Clinical Interview for DSM-IV. RESULTS: Comparison of diagnoses derived from these two approaches generated an overall kappa coefficient of .67. Kappa coefficients for the schizophrenia cohort were .94, .68 for the major depressive disorder cohort, and .58 for the bipolar disorder cohort. CONCLUSIONS: Thus, although it may be sufficient to establish the postmortem diagnosis of schizophrenia using one of the two methods, the best method for reaching an accurate postmortem diagnosis for mood disorders is more difficult to determine and requires further study.

Postmortem investigations of the pathophysiology of schizophrenia: the role of susceptibility genes.

Despite robust evidence for the heritability of schizophrenia, postmortem studies have not traditionally linked cellular and molecular neuropathology with underlying genetic mechanisms in this disorder. The completion of the first draft of the Human Genome Project and the use of novel strategies in studying complex genetic disorders including schizophrenia have led to the identification of a growing list of schizophrenia susceptibility genes. In this review, we describe the strategy used to incorporate 2 potential schizophrenia susceptibility genes in the postmortem investigation of the pathophysiology of schizophrenia driven by 2 well-established hypotheses, the dopamine hypothesis and the neurodevelopmental hypothesis. The first gene codes for catechol-O-methyltransferase, an enzyme involved in catecholamine degradation, and the second gene codes for brain-derived neurotrophic factor, a growth factor implicated in cell survival, synaptogenesis and the development of cortical pyramidal neurons.

Variation in GRM3 affects cognition, prefrontal glutamate, and risk for schizophrenia.

GRM3, a metabotropic glutamate receptor-modulating synaptic glutamate, is a promising schizophrenia candidate gene. In a family-based association study, a common GRM3 haplotype was strongly associated with schizophrenia (P = 0.0001). Within this haplotype, the A allele of single-nucleotide polymorphism (SNP) 4 (hCV11245618) in intron 2 was slightly overtransmitted to probands (P = 0.02). We studied the effects of this SNP on neurobiological traits related to risk for schizophrenia and glutamate neurotransmission. The SNP4 A allele was associated with poorer performance on several cognitive tests of prefrontal and hippocampal function. The physiological basis of this effect was assessed with functional MRI, which showed relatively deleterious activation patterns in both cortical regions in control subjects homozygous for the SNP4 A allele. We next looked at SNP4's effects on two indirect measures of prefrontal glutamate neurotransmission. Prefrontal N-acetylaspartate, an in vivo MRI measure related to synaptic activity and closely correlated with tissue glutamate, was lower in SNP4 AA homozygotes. In postmortem human prefrontal cortex, AA homozygotes had lower mRNA levels of the glial glutamate transporter EAAT2, a protein regulated by GRM3 that critically modulates synaptic glutamate. Effects of SNP4 on prefrontal GRM3 mRNA and protein levels were marginal. Resequencing revealed no missense or splice-site SNPs, suggesting that the intronic SNP4 or related haplotypes may exert subtle regulatory effects on GRM3 transcription. These convergent data point to a specific molecular pathway by which GRM3 genotype alters glutamate neurotransmission, prefrontal and hippocampal physiology and cognition, and thereby increased risk for schizophrenia.