NEUROANATOMICAL AND NEUROPHYSIOLOGICAL MECHANISMS INVOLVED IN CENTRAL-NERVOUS-SYSTEM DYSFUNCTIONS INDUCED BY PRENATAL ALCOHOL EXPOSURE

One of the most severe consequences of maternal ethanol consumption is :he damage to the developing central nervous system, which is manifest ed by long-term cognitive and behavioral deficits in the offspring. Pr enatal exposure to ethanol affects many crucial neurochemical and cell ular components of the developing brain. Ethanol interferes with all o f the stages of brain development, and the severity of the damage depe nds on the amount of ethanol intake and level of exposure. Experimenta l observations also indicate that the toxic effects of ethanol are not uniform: some brain regions are more affected than others and, even w ithin a given region, same cell populations are more vulnerable than o thers. The neocortex, the hippocampus, and the cerebellum are the regi ons in which the neurotoxic effects of ethanol have been associated wi th the behavioral deficits. At the cellular level, ethanol disrupts ba sic developmental processes, including interference with division and proliferation, cell growth, and differentiation and the migration of m aturing cells, Alterations in astroglia development and In neuronal-gl ial interactions may also influence the development of the nervous sys tem, An impairment of several neurotransmitter systems and/or their re ceptors, as well as changes in the endocrine environment during brain development, are also important factors involved in the behavioral dys functions observed after prenatal ethanol exposure. Finally, some mole cular mechanisms of ethanol-induced behavioral dysfunctions will be di scussed.