Studies have shown that while HAP-1 mice consume two to three times more alcohol than LAP-1 mice (Grahame et al., 1999a), LAP-1 mice showed greater alcohol withdrawal severity following acute alcohol exposure (Chester et al., 2003). These differences between HAP-1 and LAP-1 mice are consistent with differences in alcohol consumption between B6 and D2 mice. However, the electrophysiological profile distinguishing HAP-1 from LAP-1 mice (Slawecki et al., 2003) differs from our earlier results characterizing B6 and D2 mice (Ehlers and Somes, 2002). We previously showed that HAP-1 mice had significantly larger amplitude in the P1 ERP component compared to LAP-1 and HS/Ibg mice (Slawecki et al., 2003). This increased P1 amplitude in the frontal cortex was one of the neurophysiological variables that differentiated HAP-1 from LAP-1 mice. In addition, we showed that EEG peak frequency was lower in LAP-1 mice in the 2–4 Hz and 8–16 Hz EEG bands of the frontal cortex, compared to HAP-1 mice (Slawecki et al., 2003). In contrast, average cortical EEG power was not different between HAP-1 and LAP1 mice (Slawecki et al., 2003). These
