Ethanol, Stroke, Brain Damage, and Excitotoxicity

摘要: The N-methyl-d-aspartate (NMDA)-glutamate receptor could contribute to stroke, trauma, and alcohol-induced brain damage through activation of nitric oxide formation excitotoxicity. In rat primary cortical cultures NMDA was more potent at activating than triggering Ethanol dose dependently inhibited both responses. contrast, treatment neuronal with ethanol (100 mM) for 4 days significantly increased stimulated These findings suggest that acutely inhibits but chronically causes supersensitivity NMDA-induced excitotoxicity in cultures. To investigate ethanol's interaction stroke induced models global cerebral ischemia were studied. Transient resulted a loss hippocampal CA1 pyramidal neurons over 3- 5-day period. Determinations the ligand binding stoichiometry or postischemic changes did not show differences between undergo delayed death following those no toxicity, example, dentate gyrus, respectively. Acute (3 g/kg) found protect against ischemia-induced by lowering body temperature, under temperature controled conditions. studies indicate factors contributing stroke-induced are complex, although they consistent chronic increasing