The lack of alcohol effect on Ki-67+ cells following binge alcohol exposure in adolescents differs from that observed in binge alcohol-exposed adults, where Ki-67+ cells are reduced by 30% (Crews et al., 2006a). This implies a developmental difference, though subtle, in the mechanism of alcohol effects on neurogenesis. For example, the reduction in Ki-67+ cells in adults (e.g. Crews et al., 2006a) reflects that fewer cells are in the active portion of the cycle, which could be due to either loss of progenitors or cells driven to quiescence (G0 phase). As discussed above, adolescent data suggest that alcohol is arresting or altering the cell cycle, an effect that is more similar to that observed during early development (Luo and Miller, 1998). This is consistent with developmental differences in the amount of neurogenesis or increased numbers of proliferating cells in the adolescents versus adults (He and Crews, 2007). Although the length of the cell cycle is similar between adults and adolescents (Cameron and McKay, 2001), little is known about the cell cycle or the reaction of NSC to various factors during
