Morphological, neurochemical, and electrophysiological studies suggest that the hippocampal formation is one of the brain regions most sensitive to the teratological consequences of prenatal exposure to ethanol. We now report that prenatal ethanol exposure results in a reduction in the sensitivity of the hippocampi of adult offspring to N-methyl-D-aspartate (NMDA). Moreover, it appears that reduced sensitivity to NMDA results from abnormal magnesium regulation of the NMDA receptor-channel complex. These deficits in hippocampal function may underlie some of the behavioral and learning deficits which are characteristic of the offspring of mothers that consume even moderate amounts of ethanol during pregnancy.