Ethanol neurobehavioral teratogenesis and the role of the hippocampal glutamate-N-methyl-D-aspartate receptor-nitric oxide synthase system

The purpose of this review is to evaluate a proposed mechanism for ethanol neurobehavioral teratogenesis in the hippocampus, involving suppression of the glutamate-N-methyl-D-aspartate (NMDA) receptor-nitric oxide synthase (N OS) system. It is postulated that suppression of this signal transduction s ystem in the fetus by chronic maternal consumption of ethanol plays a key r ole in hippocampal dysmorphology and dysfunction in postnatal life. This me chanism is evaluated critically based on the current literature and our res earch findings. In view of the apparent time course for loss of CAI pyramid al cells in the hippocampus produced by chronic prenatal ethanol exposure t hat manifests in early postnatal life, it is proposed that therapeutic inte rvention, which targets the glutamate-NMDA receptor-NOS system, may prevent or lessen the magnitude of postnatal hippocampal dysfunction. (C) 2000 Els evier Science Inc. All rights reserved.