These data are the first to show a decrease in neurogenesis in an adolescent rat model of an AUD. Specifically, binge alcohol exposure in adolescent rats reduced DCX+IR, a widely accepted marker of neurogenesis (Figure 2; Rao and Shetty, 2004). To further probe for mechanism of alcohol-induced inhibition of neurogenesis, a systematic assessment of the different aspects of neurogenesis was conducted. First, the decrease in DCX expression corresponded to reduced cell proliferation as evidenced by a decrease in BrdU-labeling of cells in S-phase immediately after the last dose of alcohol (Figure 3). Second, newborn cell survival was impacted as shown by the significantly reduced percentage of BrdU labeled cells that remain or survive to 28 days after the last dose of alcohol (Figure 6). As alcohol exposure did not alter the differentiation of newborn cells, when cell counts at 4D+28 (Figure 6) were combined with phenotype percentages (Figure 5), a nearly 50% reduction in neurogenesis was estimated at four weeks after the last dose of alcohol. Although the loss of BrdU+ signal at D4+28 days could in theory be due
