Other patterns of AE-induced neurotransmitter-specific gene responses involve persistent changes in adulthood, but varied adolescent brain responses (Fig. 4, Table 1). Although AE decreased expression in general, gene specific reductions in expression levels were often not statistically significant at P38. Following ethanol treatment, most genes followed a decreasing developmental trajectory similar to that found in controls (Fig. 4 and Table 1). Gastrin releasing peptide receptor, Grpr, was unique among the transmitter genes studied, in that its expression did not change during adolescence/early adulthood (P38-P88) or during adulthood (P98-P148) (Figure 2). Neither was Grpr expression altered 24 hours following adolescent binge ethanol, or at all (24h or 50 days) following adult binge ethanol treatment (Tables 1 and 2). However, in adults (P88) 50 days after AE binge treatment, Grpr expression was 55% of P88 controls (†p<0.05, t-test, P88 control vs P88 ethanol group), suggesting a unique adolescent-specific ethanol effect. Other mRNAs that were not markedly altered on P38 just after AE binge treatment, but showed statistically significant reductions 50 days after AE treatment (P88) were cholecystokinin α and β (CCKα and
