Taken together, the cellular alterations produced by both moderate (nondependent) and excessive (dependent) alcohol use may be extended into other behavioral effects of alcohol addiction. For example, human alcoholics are known to suffer from hippocampal-dependent cognitive deficits, including impulsivity and deficits in spatial learning, short-term memory, and executive function (Uekermann et al., 2003), possibly reflecting chronic alcohol-induced decreased hippocampal neurogenesis. Although we do not provide a direct link to demonstrate that hippocampal neurogenesis is a vulnerability factor for alcohol dependence (Meshi et al., 2006), we demonstrate that altered plasticity in the mPFC and SGZ produces neuroadaptations in the PFC and hippocampus that may contribute to increased alcohol-drinking or may perpetuate excessive alcohol drinking.
