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 electrophysiological findings suggest that increased P1 amplitude and increased delta and alpha EEG peak frequencies are the most likely variables indexing susceptibility to high alcohol consumption and preference in ‘high risk” HAP-1 mice compared to ‘low risk’ LAP-1 mice. The P1 component is a large positive component that peaks between 45 and 60 ms (Slawecki et al., 2003). In our original ERP study (Slawecki et al., 2003), assessment of the neurophysiological profile in HS/Ibg mice allowed for the determination of which line, the HAP-1 or the LAP-1, deviated most from the progenitor stock. These initial studies found that HAP-1 mice consumed more alcohol and had higher alcohol preference than LAP-1 and HS/Ibg mice (Slawecki et al., 2003). P1 amplitude was greater in HAP-1 mice than in LAP-1 and HS/Ibg mice (Slawecki et al., 2003). In contrast, the present study found that HAP-1, LAP-1 and HS/Ibg mice showed no significant differences in ERO energy in the delta, theta and alpha/beta bands
