Teratogenic effects of alcohol have been documented for nearly forty years since Smith and Jones (1973) first defined the clinical features of Fetal Alcohol Syndrome (FAS). Ethanol consumption during pregnancy continues to be a problem; 12.5 % of women drink while pregnant (CDC, 2009) with the prevalence of FAS estimated at 1% of live births (May and Gossage, 2001, Sampson et al., 1997) and associated care costs estimated at nearly 4 billion dollars annually in the US alone (Lupton et al., 2004). It is now recognized that ethanol exposure during development can produce a spectrum of behavioral and cognitive deficits, referred to as Fetal Alcohol Spectrum Disorders (FASD) (Manning and Hoyme, 2007, Riley and McGee, 2005, Streissguth et al., 1996). Executive functioning deficits commonly reported in FASD patients (Connor et al., 2000, Kodituwakku, 2009, Rasmussen, 2005) can in turn result in deficits in social behaviors and increases in high risk behaviors such as drug use (Connor et al., 2000, Olson et al., 1997). Consistent with this relationship, individuals with FASD are impaired in social behavior to a greater extent than
