levels persist longer in humans than mice (Thurman et al., 1982; Bradford et al., 2007). Our adolescent binge ethanol treatment followed by assessments in young adults mimics the “young adult alcohol dependent subtype,” the most common alcohol dependence subtype characterized by heavily drinking during adolescence -young adulthood, and maturation out of dependence (Jacob et al., 2005; Moss et al., 2007). Although it is of interest to distinguish adolescent from adult responses, since human adolescents represent the majority of binge drinkers, understanding the persistent effects of adolescent binge ethanol on the adult brain may be the most important for human health considerations. Therefore, though we compared the effects of binge ethanol during adolescence with that of adults on neurotransmitter receptor genes, we focused the remainder of our analyses on the persistent effects of the adolescent binge. Our model replicates rat models of binge drinking that did not demonstrate changes in locomotor activity (Slawecki et al., 2001), water maze spatial learning (Schulteis 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
