PubMed · 4639594
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J A Meerloo. 1972-11-18. [Psychologic dizziness].. https://pubmed.ncbi.nlm.nih.gov/4639594/
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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.
The effects of early environmental influences on neural plasticity, the limbic system, and social and emotional development are reviewed and an illustrative case study is briefly discussed. Deprived or abnormal rearing conditions induce severe disturbance in all aspects of social and emotional functioning, and effect the growth and survival of dendrites, axons, synapses, interneurons, neurons, and glia. The amygdala, cingulate, and septal nuclei develop at different rates which correlate with the emergence of wariness, fear, selective attachments, play behavior, and the oral and phallic stages of development. These immature limbic nuclei are "experience-expectant," and may be differentially injured depending on the age at which they suffer deprivation. The medial amygdala and later the cingulate and septal nuclei are the most vulnerable during the first three years of life. If denied sufficient stimulation these nuclei may atrophy, develop seizure-like activity or maintain or form abnormal synaptic interconnections, resulting in social withdrawal, pathological shyness, explosive and inappropriate emotionality, and an inability to form normal emotional attachments.
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