Conversely, the hypothesis that AAU actively reduces P300 amplitude predicts that the G-E interplay underlying P300 amplitude is contextually dependent on AAU history. This would occur because the contribution of A and E to P300 amplitude variability depends on the extent of alcohol consumption. However, the mechanisms underlying the possible neurotoxicity of alcohol on adolescent brain development are not well established and thus it is not clear how the contribution of A and E to P300 amplitude would vary with the amount of alcohol consumed. It is possible to present idealized plausible alternatives that illustrate how alcohol consumption might moderate G-E interplay. Because increased alcohol consumption is associated with diminished P300 amplitude, it is reasonable to assume that with increasing alcohol consumption, the variability evident in P300 amplitude increases by rendering P300 smaller than it would otherwise be in the absence of alcohol consumption. Hence, both Figures 1b and 1c posit increases in the overall variability in P300 amplitude with increasing alcohol consumption. Figure 1b illustrates what we might expect if alcohol consumption increases the genetic variability in P300 amplitude
