In the hippocampal dentate gyrus, chronic intermittent alcohol exposure markedly reduced proliferation, as detected both by BrdU-IR and Ki67-IR. Because Ki67 measures were highly correlated with those for BrdU and produced the same temporal profile, it is unlikely that effects on circulation or integrity of the blood–brain barrier, that could otherwise affect BrdU incorporation, could confound our proliferation estimates. Furthermore, neurogenesis, detected as DCX-IR, was also suppressed at the end of alcohol exposure. These data are in agreement with published reports, which consistently find that hippocampal neurogenesis in rats is reduced by alcohol upon voluntary self-administration (Crews et al. 2004; Stevenson et al. 2009), combined vapour inhalation and self-administration (Richardson et al. 2009), and after a 4-d binge-like dependence model (Nixon & Crews, 2002). Our present findings demonstrate that suppression of hippocampal neurogenesis occurs with prolonged dependence, and does not recover as long as intoxicating blood alcohol levels are maintained.
