PubMed · 4760948
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S Verret. 1973. [The minimal brain dysfunction syndrome].. https://pubmed.ncbi.nlm.nih.gov/4760948/
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The purpose of this paper is to provide a concise, selective review of the major issues and findings germane to structural and functional neuroimaging studies of bipolar affective disorder (BPD). In attempting to identify the brain changes associated with BPD, investigators have used neuroimaging techniques to focus on several interrelated questions. These are: What are the changes and where do they occur? Do their nature and location suggest a particular etiopathologic basis or have notable clinical correlates? With regard to specificity, are the changes unique to BPD, or do they overlap with those reported in other neuropsychiatric illnesses, especially schizophrenia? Do they occur in brain systems that normally play a role in modulating mood? Finally, how do the brain changes integrate with neurocognitive, neurogenetic, and neuropathologic data in the same patients? To date, these questions have been addressed only preliminarily. We outline some of the strategies used to pursue answers to these questions and review conclusions to date.
In this article, post-mortem neurohistological and structural imaging studies of schizophrenia and mood disorders are briefly reviewed. In contrast to the large number of post-mortem studies on schizophrenia published during the last 20 years, very few histological studies of affective disorders are available. After commenting on CT and MRI studies, as well as on neuropathological findings on whole-brain size, cortex, frontal and temporal lobes, limbic system, basal ganglia, thalamus, brain stem, and cortical asymmetry, it is concluded that despite a broad overlap in structural findings in the so-called endogenous psychoses, heteromodal association cortex, limbic system, and structural asymmetry are more affected in schizophrenia, while subtle structural abnormalities in the basal ganglia, especially in the nucleus accumbens and in hypothalamic areas, might play a crucial role in mood disorders.
Mice lacking Fyn, a Src-related non-receptor tyrosine kinase, show impairment of various behaviors, such as spatial learning, suckling, emotional behaviors, and ethanol sensitivity. These mice also display both morphological defects and impairment of synaptic function. Fyn is highly expressed in the mammalian CNS from embryonic day 8.5 to adulthood. Pharmacological and electrophysiological analyses of mice lacking Fyn reveal gamma-aminobutyric acid and glutamatergic defects. We propose here the hypothesis that these defects are caused separately by developmental disorganization and impairment of synapse function by a deficit in Fyn. Regarding the glutamatergic defect, in particular, after ethanol administration the N-methyl-D-aspartate (NMDA)-dependent function is recovered by Fyn, paralleled with tyrosine phosphorylation of NMDA receptor 2B subtype. Thus, modulation of the NMDA receptor function by Fyn may have a significant role in building and regulating sophisticated neural circuits and behavior. In addition, the cadherin-related neural receptor (CNR) family is isolated by binding activity for Fyn. The CNR-Fyn complex will also open a new angle for gaining insight into the molecular mechanisms for regulating mammalian behavior.