It has been hypothesized that an underlying CNS disinhibition (i.e., hyperexcitablity) is involved in a predisposition to develop alcoholism (Begleiter and Porjesz, 1999). As described earlier, low-amplitude P3 in alcoholics is also suggestive of reduced CNS inhibition. A collection of studies examining offspring of alcoholics who are at greater risk has helped to understand if the low P3 amplitudes are due to prolonged effects of alcohol on the brain, or if they are antecedent to its development, indicating an underlying predisposition. Young HR sons of alcoholics without prior alcohol exposure had significantly lower P3 voltages compared with matched LR boys from control families without first- or second-degree alcoholic relatives (Begleiter et al., 1984). These findings were replicated in many HR/LR samples (older/younger, male/female) under several experimental conditions (for review, see Porjesz et al., 2005). Furthermore, low P3 amplitude prior to puberty has been found to predict later substance abuse, including alcohol abuse in adolescence (Berman et al., 1993; Hill et al., 1995b; Iacono et al., 2002, 2003). In addition to P3b results, offspring of alcoholics also manifested low-amplitude P3a components in both visual (Rodriguez Holguin et al., 1999) and auditory paradigms (Hada et al., 2001).
