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 adolescent rats demonstrate more persistent alcohol effects for many plasticity-related and cytoskeletal proteins [34,49]. Considering that hippocampal neurodegeneration is more consistently observed in adolescents with AUDs than adults, alcohol inhibition of adult neurogenesis - or degeneration through lack of cell generation - may explain the vulnerability of the adolescent hippocampus to alcohol-induced neurodegeneration [38].
