The effects of alcohol on proliferation of cortical precursors has been studied in vitro, in which alcohol decreased proliferation of cultured neocortical neurons (Jacobs and Miller, 2001). The present study demonstrates the dynamic regulation of adult mPFC proliferative capacity and underscores the specific influence that alcohol dependence has on cell birth, survival, and death in vivo. Alcohol dependence reduced proliferation and survival in the mPFC, suggesting that the level of alcohol exposure was critical for producing changes in the gliogenic integrity of the mPFC. Decreased survival of mPFC cells may be due to decreases in S phase cells during BrdU incorporation or decreased maturation and survival of S phase cells with chronic alcohol exposure. Ki-67 analysis suggests that the former mechanism is true, albeit further studies incorporating a time course of BrdU labeling are needed to detect the latter mechanism. Additional labeling studies with phenotypic makers for immature neurons, mature neurons, astrocytes and oligodendrocytes in the mPFC will also allow us to delineate specific effects of alcohol dependence on the phenotype of surviving cortical precursors. Nondependent drinking showed a trend
