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 network regions (Northoff et al., 2007) that here demonstrated decreased vigilance and increased fixation response in FHP youth. Northoff et al. (2007) reported that GABA concentration predicted the magnitude of negative BOLD response (relative to a resting state) in the anterior cingulate. Additionally, the anterior and posterior cingulate gyri and medial frontal gyri have been indicated as potential sources of the P300. For instance, Ardekani et al. (2002) found a correlation between event-related potentials and BOLD activation to a visual odd-ball task. However, studies mapping anatomical origins of electrophysiological data have yet to reach consensus. Nonetheless, an intriguing body of emerging evidence suggests that suboptimal modulation of default networks in response to cognitive demands may relate to atypical electrophysiological activity and behavioral disinhibition in nondrinking FHP individuals.
