Clinical assessments of people with FASD have suggested that executive dysfunction results in impairments in everyday functioning including social behavior and increased risk for drug and alcohol abuse (Connor et al., 2000, Olson et al., 1997). The current findings suggest a disruption of processing in the mPFC which may be relevant to these behavioral impairments. The current data indicate a selective sparing of medium spiny neurons in the NAC from teratogenic effects of ethanol while layer II/III pyramidal neurons of the mPFC had reductions in spine density, changes in spine distribution, and increased soma size. Taken together with previous findings from both our laboratory and others, it suggests that secondary effects, such as impaired social behavior and substance abuse, may be the result of alterations in the morphology of the mPFC and activity but not morphology of the NAC. Further experimental investigation into the impact of ethanol exposure during development on the NAC and mPFC would provide a greater understanding of mechanisms of complex secondary effects and insights with respect to treatment possibilities in FASD.
