punctate D4DR+IR that was 44% less in the OFC of P38 binge ethanol treated mice compared to P38 adolescent control mice (Figure 3, *p<0.05). Since the developmental decrease in D4DR mRNA mimicked the AE induced decrease and no developmental change occurred in ethanol treated animals, D4DR gene expression was similar in P88 controls and P88 ethanol treated animals (Figure 3A). Both punctate and somatic D4DR+IR staining were observed in adults, suggesting developmental regulation of D4DR subcellular localization (Figure 3). There was no effect of adult ethanol binge treatment (P88-P97) on D4DR gene expression either immediately (P98) or after 50 days (P148). Thus, D4DR development is disrupted by adolescent binge ethanol treatment, although expression levels in adults appear normal.
