in the array, 58 were persistently reduced by binge ethanol treatment at P88 (Table 1, *p<0.05, **p<0.01 t-test, P38 control vs P88 ethanol), and 31 after Bonferroni correction for multiple comparisons (Table 1, §p<0.05 Bonferroni post-test). Regarding the 15 cholinergic genes, expression in young adult controls (P88) averaged 37% (range 23-75%) of control adolescent (P38) levels with no single gene significantly decreased (Table 1). AE binge treatment significantly altered cholinergic genes. Cholinergic gene expression in young adults (P88) that received AE binge averaged 20% (range 14-45%) of control P38 levels, with 11 of the 15 cholinergic genes showing significant reductions (Table 1, §p<0.05 Bonferroni post-test). Adults (P148) 50 days following an earlier adulthood ethanol binge (P88-P97, Figure 1) also showed signs of an enhanced reduction in neurotransmitter-specific gene expression (Table 2; p<0.0001, F=40.18). However, the reduction was much less than that found in the adolescent binge treated group (average reduction of 37% vs 73% reduction following AE binge). Also, only two individual genes were suppressed persistently at P148 following young adult binge ethanol treatment (P88-P97): CCKα and Galantin receptor 2 (Table 2; 56% and 55% reduction respectively, *p<0.05 t-test). The statistical significance of these two reductions was lost after Bonferroni
