further decreased after prolonged dependence, suggesting that minimal levels (threshold) of proliferation is persistent in the hippocampal SGZ, and that continued chronic alcohol exposure does not disrupt this threshold of proliferation. Note that immature neurons were further reduced only in the dependent group suggesting that dependence-induced decreases in neurogenesis were due to more robust effects on differentiation and maturation of hippocampal progenitors. Thus it appears that progression of dependence targets distinct population of progenitors, where proliferation is initially altered, followed by alteration in differentiation and maturation of progenitors, ultimately leading to decreased hippocampal neurogenesis.
