Thus far, only a handful of studies have actually examined more than one or two of these rat lines to determine whether the findings are generalizable or not. Nevertheless, findings from these few studies support the hypothesis that these animal models, as a group, display some of alcoholism’s clinical-like heterogeneity. One clear distinction can be made between the genotypes of P vs. NP and HAD vs. LAD line-pairs, such that QTLs associated with alcohol preference are on chromosomes 3, 4 and 8 for the P vs. NP line-pair, whereas the QTLs are located on chromosomes 5, 10, 12 and 16 for the HAD1 vs. LAD1 and chromosomes 10 and 16 for the HAD2 vs. LAD2 line-pairs. Understandably, candidate genes associated with the alcohol preference phenotype also differ between these line-pairs, with NPY, alpha synuclein (Snca) and the CRF2 receptor (Liang et al., 2003; Spence et al., 2009) as well as preproNPY (c.f., Koob and Le Moal, 2006) on chromosome 4 for the P vs. NP line-pair and CREB binding protein (Crebbp) and a MAP kinase (Mapk8ip3) on chromosome 10 (Bice
