Studies have demonstrated that, relative to NP rats, the P rat exhibit several phenotypes associated with alcohol abuse and alcoholism and meets the criteria of a valid animal model to assess alcohol-preference and excessive drinking (for review, see McBride et al., 2005; Bell et al., 2006). Consistent with studies in human subjects at risk for ethanol dependence (for review see Porjesz et al., 2005), our previous study showed that P rats have significantly lower P3 amplitude, when compared to NP rats (Ehlers et al., 1999). However, the relationship between an ethanol preference phenotype and changes in EROs are not well understood in genetic mouse models of high and low alcohol preference. There is evidence to suggest that multiple neurotransmitter systems contribute to differences in ethanol preference between P and NP rats (for review, see McBride et al., 2005; Bell et al., 2006). For instance, early-onset of ethanol drinking in P rats has been associated with higher density of cortical and hippocampal seronin-1A (5-HT1A) receptors and lower density in the expression of dopamine (DA) D2 receptors in the ventral tegmental area
