It is well-accepted that neural stem cells produce new neurons in the dentate gyrus of the hippocampus throughout life as an integral process to hippocampal structure and function [59]. Recent work suggests that alcohol effects on neural stem cells may underlie the susceptibility of the adolescent hippocampus to alcohol-induced degeneration [10,38]. Acutely, alcohol inhibits adult neurogenesis by reducing neural stem cell proliferation [38]. However, in models of an AUD, alcohol both impairs neural stem cell proliferation and reduces survival of newborn neurons [10]. By our estimates, alcohol inhibition of adult neurogenesis eliminates thousands of hippocampal neurons, whereas cell death only eliminates a few hundred. This loss is due to the developmental state of the adolescent brain where the number of new neurons produced is many-fold higher than in adults [60]. Thus, because of the higher rate of neurogenesis in adolescents, a greater number of cells are “lost” (never born or survive) due to alcohol as opposed to adults [10,38]. The enhanced vulnerability of the adolescent brain to alcohol-induced effects on a form of plasticity is consistent with recent observations that
