Basic animal model studies have established that high blood levels of alcohol can induce brain damage (Crews et al., 2004). Many studies of alcohol induced brain damage have used a multiday binge induced brain damage model in rats. This model involves high blood ethanol levels (≅ 250mg %) that are similar to the blood alcohol levels commonly found among hospital emergency room patients (Teplin et al., 1989). In the binge model alcohol induced brain damage occurs during intoxication in limbic and frontal cortex, including agranular insular cortex, anterior piriform cortex, perirhinal cortex, entorhinal cortex and hippocampal dentate gyrus, particularly ventral dentate gyrus (Fig. 3). Dark cell degeneration, a necrotic form of cell death with shrunken soma is the predominant form of neuronal death (Obernier et al., 2002a). In addition, ethanol inhibits brain neural stem cell proliferation and neurogenesis (Fig. 3) (Nixon and Crews, 2002), possibly contributing to deficits in learning and alterations in mood (Crews et al., 2003; Stevenson et al., 2008). In general the diffuse degeneration and loss of neurogenesis found in the rat binge model mimics the diffuse
