It was a turning point in alcoholism research that lower P3 amplitude, observed in alcoholic individuals (Porjesz and Begleiter, 1981; Oscar-Berman, 1987; Pfefferbaum et al., 1987; Porjesz et al., 1987; Cohen et al., 1995; Cohen et al., 1997b; Rodriguez Holguin et al., 1999a; Hada et al., 2000; Prabhu et al., 2001; Cohen et al., 2002; Suresh et al., 2003; Kamarajan et al., 2005a; Fein and Chang, 2006; Kamarajan et al., 2010; Fein and Andrew, 2011), was also found in individuals with a family history of alcoholism who were considered to be genetically vulnerable but had not yet developed alcoholism (Elmasian et al., 1982; O’Connor et al., 1987; Porjesz and Begleiter, 1990; Benegal et al., 1995; Porjesz et al., 1996; Ramachandran et al., 1996; Kamarajan et al., 2005b) and had never or only rarely been exposed to alcohol (Begleiter et al., 1984; Begleiter et al., 1987; Whipple et al., 1988; Whipple et al., 1991; Hill and Steinhauer, 1993; Steinhauer and Hill, 1993; Hill et al., 1995). However, it must be stated that P3 reduction in high risk subjects, as a phenomenon,
