Evidence suggests that adolescent alcohol use (AAU), a robust correlate of adult alcoholism (Anthony & Petronis, 1995; Brown & Tapert, 2004; DeWit, Adlaf, Offord, & Ogborne, 2000), may represent one such deleterious environment. Animal research has related ethanol exposure to neurodevelopmental damage, both in terms of structure (e.g. hippocampus, frontal lobes) and function (e.g. thermoregulation, balance, memory; Brown & Tapert, 2004; Crews, Braun, Hoplight, Switzer, & Knapp, 2000; Hiller-Sturmhofel & Swartzwelder, 2004; White & Swartzwelder, 2004). Additionally, a variety of neurobiological deficits have been reported for human adolescents with alcohol use disorders on neuropsychological measures (Brown, Tapert, Granholm, & Delis, 2000; Moss, Kirisci, Gordon, & Tarter, 1994; Sher, Martin, Wood, & Rutledge, 1997) and in brain structure and function (De Bellis et al., 2000; De Bellis et al., 2005; Tapert et al., 2001). Thus, while P3AR may index genetic risk for alcoholism prior to alcohol exposure (Begleiter et al., 1984; Viana-Wackermann et al., 2007), AAU may also reduce P300 amplitude. This scenario represents an alternative, environmentally based explanation for why P3AR is often associated with risk for alcohol misuse in
