effects (Almasy et al., 1999; Almasy et al., 2001). In addition, using the same paradigm, Roopesh et al. (2009) found that high risk offspring of alcoholics compared to low risk children showed a similar lack of N400 attenuation for primed words observed in the alcoholics in this study. Similarly, in another semantic priming study, alcoholic subjects with positive parental history compared to alcoholic subjects with negative parental history showed impairment for associated targets (Sayette et al., 2001). Among the several features required to meet criteria for an endophenotype (Gottesman and Shields, 1972, 1973; Gottesman and Gould, 2003) affected individuals (newly diagnosed, abstinent/chronic alcoholics) should manifest the trait, and the trait must be present in unaffected relatives of affected individuals with levels significantly higher than in random controls. Given our results of the lack of N400 attenuation for primed words and the deficits in discriminating between primed and unprimed words in both adult alcoholics and the offspring of alcoholics, it is suggested that N400 may have great utility as an electrophysiological endophenotype that characterizes genetic vulnerability to alcohol dependence. Future work examining the correlations between P3 amplitude changes and N400 attenuation would help to determine if similar or independent processes underlie
