possible that a burst in neurogenesis was missed by the time-points chosen (Brown et al. 2003). Alternatively, following prolonged rather than acute brain alcohol exposure, increased proliferation may to a lesser extent result in formation of new neurons that differentiate and survive. This could be caused by decreased survival of newly generated cells, as previously shown with prolonged brain alcohol exposure (Herrera et al. 2003), or decreased differentiation of progenitors into neuronal phenotypes following prolonged dependence. Finally, 1 and 3 wk into abstinence, both proliferation rates and neurogenesis in the dentate gyrus had returned to normal, indicating that effects of alcohol dependence in this region are transient and ultimately reversible.
