et al., 2008; White et al., 2002) or elevated plus maze performance (White et al., 2002). We found alterations in reversal learning in young adult mice after adolescent binge treatment, consistent with an adult rat binge drinking model (Obernier et al., 2002). Reversal learning deficits have been observed in human alcoholics (C. B. Fortier et al., 2008), cocaine addicts (Fortier et al., 2008; Stalnaker et al., 2009) and neurodegenerative diseases (Freedman and Oscar-Berman, 1989; Oscar-Berman and Zola-Morgan, 1980). Frontal cortex, where we found altered adolescent D4DR expression, and marked rat adolescent binge brain damage (Crews et al., 2000a), is implicated in drug dependence and reversal learning deficits (Schoenbaum et al., 2009). Reversal learning deficits have also been observed in rats and marmosets following lesions of the basal forebrain (Cabrera et al., 2006; Roberts et al., 1992; Tait and Brown, 2008). Our finding suggests that individuals who drink heavily during adolescence may be more likely to have reversal learning deficits, possibly mediated by chemical or structural changes in frontal cortex or basal forebrain.
