A consistent picture thus emerges for the effects of prolonged brain exposure to intoxicating alcohol levels on hippocampal neurogenesis. During chronic intoxication, the rate of new neuron formation is markedly suppressed, presumably in part secondary to suppressed proliferation of neural precursor cells. During protracted abstinence, hippocampal rates of new neuron formation return to normal, but do not significantly rebound to compensate for the deficit that has accumulated during prolonged intoxication. The contribution of new dentate neurons has been postulated to be important for restraining stress reactivity (Mirescu & Gould, 2006), and its deletion through disruption of the gene encoding TrkB results in a highly anxious phenotype (Bergami et al. 2008). This predicts that a deficit in new dentate neurons following prolonged alcohol dependence might contribute to exaggerated stress reactivity and elevated anxiety in the post-dependent state, a behavioural phenotype that is in fact consistently observed (Heilig & Koob, 2007).
