PubMed · 7350071
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K M Heilman, E Valenstein. 1980. Emotional disorders caused by CNS dysfunction.. https://pubmed.ncbi.nlm.nih.gov/7350071/
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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.
BACKGROUND/PURPOSE: Little is known about the long-term psychosocial functioning of children with esophageal atresia (EA). The physical, psychological, and social functioning of children with EA was studied using standardized assessment procedures, and relations between medical and social background variables and outcome were investigated. METHODS: Subjects were 36 children (20 boys, 16 girls; mean age 10.2 years) with EA. Fourteen children had minor and 11 children had major associated congenital anomalies. According to the "Montreal" classification, eight children with major congenital anomalies who also had been dependent on artificial ventilation as newborns fell into the high-risk class. The children were subjected to an intelligence test. Parents completed standardized questionnaires concerning emotional and behavioral problems, psychosocial stress, and family functioning; children completed questionnaires concerning depression and self-esteem; and teachers completed questionnaires concerning emotional and behavioral problems. Results were compared with normative data from the general population, and correlations between background and outcome variables were computed. RESULTS: According to Desjardins' classification, 16 children had excellent, nine children had good, and four children had fair outcome. The mean intelligence quotient (IQ) of the children was 90.2, which is almost 10 points lower than the standardized norm of 100 (P < .01). High-risk children (n = 7) had a significantly lower IQ (mean IQ, 79.4; P < .05). Five times as many children (n = 8; 22%) as in the general population (4%) required special education (P < .001). More than twice as many children (30% to 35%) as in the general population (15%) showed elevated rates of emotional and behavioral problems as reported by parents and teachers (P < .02). The children did not report more negative self-esteem or more depressive symptoms than children in the general population. Children with a lower IQ reported lower scholastic competence (r = .38, P < .05) and showed more emotional and behavioral problems as reported by teachers (r = -.43, P < .05). Family functioning and levels of psychosocial stress were the same as in the general population. Children in worse functioning families showed more emotional and behavioral problems as reported by parents (r = .37, P < .05) and higher depression scores as reported by themselves (r = .47, P < .01). CONCLUSIONS: In a follow-up study using standardized assessment procedures, it was shown that children with EA have more learning, emotional, and behavioral problems than children in the general population. A high-risk group of children with major associated congenital anomalies who had been ventilated as a newborn, were at special risk for cognitive problems.
Perseverative actions are often the result of inhibitory problems; however, inhibitory problems do not always lead to perseverative actions. Some problems of inhibition have been attributed to immaturity of, or severe damage to, the prefrontal cortex. Research in this area has generally failed both to take into account species differences in prefrontal function that lead to different perseverative errors and to distinguish between perseverative errors that arise from a failure to inhibit salient emotions or motivational drives and errors that arise from an inability to engage in conceptual change. Recent studies on humans, chimpanzees, rhesus macaques, Japanese macaques, cotton-top tamarins and marmosets support this notion.