In animal models of Fetal Alcohol Syndrome, ethanol causes a number of changes in brain development, with many of these changes being very transient. This is especially true for the process of synaptogenesis in different brain areas. Our quantitative electron microscopic study of synaptogenesis in the molecular layer of the rat dentate gyrus supports the above statement, by demonstrating that ethanol has no effect on the appearance of synapses in the dentate gyrus during early postnatal life (10-30 days old). However, prenatal ethanol exposure does appear to affect the process of synapse turnover, which is indicated by the significantly delayed appearance of complex (curved) synapses and multiple synaptic contacts on single axonal terminals. Efficient synapse turnover is thought to be required for the normal maintenance of neuronal plasticity, which in turn ensures an animal's ability to respond to novel environments, tasks and injuries. It would seem that the prenatal neurotoxicology of ethanol may manifest itself by more subtle mechanisms at sites of structural and functional importance.