same subjects. Thus, although we acknowledge that this finding may reflect a Type 1 error, it is also consistent with reflecting compensatory attentional strategies in heavy drinking functional alcoholics. Finally, we observed a decrease in N2b amplitude that was about twice as large as the observed P3b amplitude reduction. Although not reported in our prior study of LTAA (Fein and Chang, 2006), we did not observe any N2 amplitude differences in that study – this is consistent with an N2 amplitude reduction being an effect of active alcohol use or abuse. This is analogous to a recent study by Martin and Garfield (2006) where alcohol administration reduced N2 amplitude (while increasing P3 amplitude – also corresponding with our observation of a marginal decrease in P3 amplitude). It is also compatible with Porjesz et al. (1987b) and Kathmann and colleagues’ (1996) observation of no difference in N2 in 14 day abstinent alcoholics. The N2 is associated with stimulus categorization, perceptual closure and attention focusing, and is thought to signal that a completed perceptual representation has been formed (Potts, 2004; Wijers et al., 1997). The more anterior fronto-central N2 is frequently interpreted as an index of response inhibition (Falkenstein, 2006; 1999) and/or
