The last stage of hippocampal neurogenesis, cell survival and maturation was visualized by injecting BrdU to label a pulse of proliferating S phase cells after which, the rats were continued in their alcohol paradigms for 4 weeks (air/vapor exposure) without further self-administration. Nondependent drinking and alcohol dependence decreased survival and neurogenesis of SGZ progenitors, and alcohol dependence reduced neurogenesis to a greater extent compared to nondependent drinking. The altered ratio in the phenotype of surviving cells after dependence suggests greater and perhaps permanent impairment of hippocampal neurogenesis due to the higher amount of alcohol exposure during dependence and long-lasting injury to the hippocampal neurogenic environment. Thus, to evaluate the effects of additional 4 weeks of continued alcohol vapor exposure on SGZ progenitors, proliferation and immature neurons were quantified from the prolonged nondependent and alcohol dependent rats. Notably, proliferation was not 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
