Animal models of FASD have indeed suggested that both the mPFC and NAC are altered by ethanol exposure during development. Ethanol exposure in rodent models of FASD occurs during the prenatal period, postnatal period or both the prenatal and postnatal period, the latter of which comprises the period equivalent to all three trimesters of brain growth in humans (Bayer et al., 1993). Prenatal ethanol exposure via liquid diet (35% Ethanol derived calories) resulted in significant reductions in cell number in layers II and V in mPFC in adult males (Mihalick et al., 2001). The mPFC cell loss was significantly correlated with executive function deficits (Mihalick et al., 2001). Complexins I and II, regulators of Ca2+ neurotransmission, were significantly reduced in the mPFC of adult rats exposed to ethanol during the prenatal period via liquid diet (36% EDC) (Barr et al., 2005). Zink et al. (2009) demonstrated similar reductions in complexin II mRNA in mPFC of young (postnatal day (PD) 8) rats exposed to ethanol from gestational day (GD) 1 to PD 8 via housing in an inhalation chamber. Given that
