The consensus from animal model studies is that “binge” effects require a long-term (multiple days) exposure to alcohol (e.g., Greiffenstein, Mathis, Stouwe, & Molina, 2007; Moore et al., 2007; Wezeman, Juknelis, Himes, & Callaci, 2007)—a viewpoint similar to the clinical alcoholic binge but quite different from the most common interpretations of binge drinking discussed above. Moreover, animal studies of alcohol binge exposure have led to the conclusion that such ethanol intake can lead to neurodegeneration in corticolimbic areas linked to learning and spatial memory (Aggleton, Hunt, & Rawlins, 1986; Haberly, 1998; Jarrard, 1993), such as the olfactory bulb, piriform cortex, perirhinal cortex, entorhinal cortex, and the hippocampal dentate gyrus (Collins, Corso, & Neafsey, 1996; Collins, Zou, & Neafsey, 1998; Corso, Mostafa, Collins, & Neafsey, 1998; Crews, Braun, Switzer, & Knapp, 2000; Zou, Martinez, Neafsey, & Collins, 1996). Researchers have found extensive neurodegeneration of the entorhinal cortex in rats after 2 days of “binge” alcohol exposure using stomach catheters that produced learning deficits (Obernier, White, Swartzwelder, & Crews, 2002). The vulnerability of this region after a single “binge” episode (i.e., 2
