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 CCKβ), and the glycine receptor α1 subunit (†p<0.05, t-test of normalized ΔCt values, P88 control vs P88 ethanol group). The pattern of developmental expression for these genes is illustrated by the peptide receptor CCKβ (Figure 4). AE binge ethanol caused a 45% decrease in CCKβR mRNA 24 hours after the end of the binge. Control animals underwent a 55% reduction in CCKβR mRNA from P38 to P88 (*p<0.05) while, ethanol treated animals underwent an additional 37% reduction in gene expression from P38 to P88, resulting in an overall 82% significant reduction from P38 control levels (§ p<0.05 Bonferroni post-test vs P38 control, †p<0.05 t-test vs P88 control). Catechol-O-methyltransferase (COMT) showed a particularly interesting pattern of altered developmental trajectory (Figure 4). Adolescent binge ethanol did not cause any change COMT gene expression at P38. Although there was a non-significant developmental reduction in controls (29% reduction, p=0.24), adolescent binge treatment resulted in a 64% significant decrease in COMT mRNA expression in P88
