Alcoholic cognitive impairments may be linked to alcoholic neurodegeneration. Investigations into the persistent behavioral effects of binge induced brain damage found that two weeks after the last dose of ethanol, binge treated rats exhibited perseverative responses in reversal learning trials (Fig. 5). (Obernier et al., 2002b). Although learning was not altered by binge treatment, Morris Water maze reversal learning, e.g. relearning tasks, showed deficits in trials to criterion, time in wrong quadrant, and entries in the wrong quadrant, that are consistent with disrupted frontal lobe function and perseveration (Obernier et al., 2002b). Animals and people with OFC lesions show reversal learning deficits (Schoenbaum and Roesch, 2005; Schoenbaum and Shaham, 2008) In addition, persistent increases in markers of microglial density, a sign of neurodegeneration, were elevated by binge rat treatment (Obernier et al., 2002b) similar to findings in post-mortem alcoholic human brain of increased microglial density (He and Crews, 2008). Thus, animal models have established that high blood alcohol levels cause neurotoxicity in cortical and limbic regions that induce reversal learning deficits that mimic the perserverative behaviors consistent with frontal cortical dysfunction in alcohol use disorders.
