Our findings have potentially interesting implications for the interpretation of anomalous electrophysiological characteristics theorized to be biological vulnerabilities for AUD and behavioral disinhibition, such as reduced P300 amplitude and increased resting beta frequency (Bauer and Hesselbrock, 1993; Hesselbrock et al., 2001; Polich et al., 1994; Porjesz et al., 2005; Rangaswamy et al., 2004a). The relationship between genetic features that determine characteristics of brain oscillations could participate in the mechanism for such predispositions. Specifically, EEG beta frequency has been linked to receptor genes for gamma-aminobutyric acid (GABA) that are involved in inhibitory neural networks (Rangaswamy et al., 2004b). The balance of inhibitory inter-neurons and excitatory pyramidal cells depends on the action of GABA subunits (Whittington et al., 2000). Because alcoholics and their children demonstrate increased beta activity, this may indicate an imbalance between excitation and inhibition (Porjesz and Rangaswamy, 2007). Variations in GABA receptor genes affect neural inhibition and thus the level of neural excitability, thereby influencing the predisposition to develop alcohol dependence and related disinhibitory disorders (Begleiter and Porjesz, 1999). Interestingly, GABA appears to specifically influence activity in the default
