Importantly, mPFC neurons project directly to the NAC with regional and laminar specificity (Basar et al., 2010, Ding et al., 2001, Brog et al., 1993) and affect NAC neuronal activity (Ishikawa et al., 2007). There have been no published studies examining neuronal structure in NAC following ethanol exposure during early development although there are findings that exposure to alcohol (Zhou et al., 2007) and other drugs of abuse (Robinson and Kolb, 1997, 1999) during adulthood reduce spine density in the NAC. Moderate ethanol exposure throughout gestation and the first two weeks postnatally failed to alter NAC volume (Rudeen, 1986) which is suggestive of no ethanol-induced changes in neuronal structure. However, there clearly are changes in the neurochemical nature of the NAC after exposure to ethanol during development. For example, perinatal ethanol exposure resulted in an increase in Met-enkephalin levels in the nucleus accumbens of female but not male rats (Lugo et al., 2006b). Male rats exposed to ethanol during the prenatal period show elevated dopamine (DA) in the NAC following self-administered ethanol compared to controls; this effect was not seen
