The majority of work looking at prenatal alcohol exposure examines its teratogenic effects on the hippocampus. For example, providing pregnant dams with a liquid diet, in which 35% of their total daily calories are provided by the alcohol (35% EDC), produces abnormal branching of the mossy fibers in the ventral hippocampus of rat pups (West et al., 1981). Along with these morphological changes, hippocampal-dependent behavioral changes are also evident after prenatal alcohol exposure. In fact, prenatal alcohol exposure has been linked with impaired spatial response-dependent learning (for review, see Berman & Hannigan, 2000). In sum, this suggests that the loss of connections in the hippocampus could be playing a role in the behavioral deficit. This relationship between changes in hippocampal structure and hippocampal-dependent behavior as a result of prenatal alcohol exposure supports the hypothesis that mPFC structural alterations may lead to PFC-dependent behavioral disabilities in patients with FASD.
