Ethanol neurobehavioral teratogenesis and the role of the hippocampal glutamate-N-methyl-D-aspartate receptor-nitric oxide synthase system.
作者： Karen A Kimura , James N Reynolds , James F Brien
DOI: 10.1016/S0892-0362(00)00089-1
关键词:
摘要: Abstract The purpose of this review is to evaluate a proposed mechanism for ethanol neurobehavioral teratogenesis in the hippocampus, involving suppression glutamate– N -methyl- d -aspartate (NMDA) receptor–nitric oxide synthase (NOS) system. It postulated that signal transduction system fetus by chronic maternal consumption plays key role hippocampal dysmorphology and dysfunction postnatal life. This evaluated critically based on current literature our research findings. In view apparent time course loss CA1 pyramidal cells hippocampus produced by chronic prenatal exposure manifests early life, it therapeutic intervention, which targets glutamate–NMDA receptor–NOS system, may prevent or lessen magnitude dysfunction.
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