(data herein; (Ieraci and Herrera, 2007; Nixon and Crews, 2002). An alternate explanation could be that the cell cycle parameters of proliferating progenitors in the dependent group are altered. For example, although Ki-67′s expression is tightly regulated and corresponds to cell proliferation (Dayer et al., 2003; Mandyam et al., 2007), some proliferating cells frozen in certain parts of the cell cycle, such as G1 (Scholzen and Gerdes, 2000) could still express the protein, suggesting that Ki-67 labeling may over-estimate proliferating cells actively progressing through the cell cycle. Because we did not observe quantitative differences in Ki-67-IR cells in the alcohol dependent group versus nondependent group, one might speculate that some Ki-67-IR cells in the dependent group may be representing the ‘trapped’ population, which inflates the number of‘proliferating’ cells observed. Additional markers would be needed to test this hypothesis. Nonetheless, it appears that exposure to even modest amounts of alcohol may cause long-term changes in the hippocampal proliferative environment, resulting in reduced neurogenic capacity in the hippocampus.
