Several alcohol models have been employed to study the effect of alcohol exposure on hippocampal proliferation. Notably, there are discrepancies on alcohol-induced effects on proliferation (Nixon, 2006), and they may be attributable to differences in alcohol delivery methods, blood alcohol levels, withdrawal time after the last exposure to alcohol prior to tissue collection, or the use of endogenous vs. exogenous markers for cell quantification. The present study utilized a clinically relevant model of dependence for adult alcoholism producing high blood alcohol levels and an endogenous marker (Ki-67) to label and quantify proliferation. Both nondependent drinking and alcohol dependence equally reduced proliferation. A lack of difference in cell proliferation between the nondependent and dependent groups could be explained by the extended exposure to alcohol self-administration in both groups, and that moderate, albeit nondependent, alcohol intake produces robust effects on hippocampal proliferation (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
