Begleiter et al. (1984) were the first to show P300 amplitude differences between high and low risk 10 year old boys who performed a visual ERP task. Numerous cross-sectional studies of ERP abnormalities in the offspring of alcohol dependent individuals and in offspring from multiplex families confirmed that reduced P300 amplitude was a plausible endophenotype for risk for AUD (Costa et al. 2000; Hesselbrock et al. 1993; Hill and Steinhauer 1993; Porjesz et al. 1998; Rangaswamy et al. 2007). Availability of data for children and adolescents studied yearly with ERP provided the first evidence that observed risk group differences might be due to altered developmental trajectories of P300 amplitude in offspring from families with high densities of alcohol dependence. Mixture analysis of trajectories suggests that those individuals with a pattern characterized by low P300 amplitude across childhood and adolescence have greater risk for externalizing disorders (Hill and Shen 2002). These findings support risk group differences in mechanisms of neural inhibition (Hill et al. 1995, 1999c).
