Another body of research shows that, similar to alcoholics, HR offspring manifest significantly lower P3 amplitude under a variety of task conditions (for reviews, see Begleiter and Porjesz 1990a,b; Porjesz and Begleiter 1990, 1991, 1997; Porjesz et al. 2005). Since the initial report of low P3 amplitudes in young sons of alcoholics prior to any exposure to alcohol (Begleiter et al. 1984), P3 deficits have been reported in both male and female children, adolescent, and young adult HR offspring (cf. Porjesz et al. 2005). It has been hypothesized that reduced P3 reflects underlying neural disinhibition (i.e., hyperexcitability), which in turn may be involved in the predisposition to alcoholism (Begleiter and Porjesz 1999). These findings underscore the utility of P3 as an effective endophenotype in alcoholism. (See more discussion on endophenotypes and genetic findings in a later section, “Electrophysiological Measures as Endophenotypes for Alcoholism.”)
