One goal of the current study was to determine if QTLs detected elsewhere for withdrawal and consumption would be confirmed in the HS4 selected lines. Metten et al. (1998a) noted that for B6×D2 crosses, there was evidence ranging from provisional to significant for reciprocal QTLs on Chr 1, 2, 4, and 15. Subsequent studies, focusing on the acute withdrawal phenotype, have confirmed QTLs on Chr 1 and 4 and an additional QTL on Chr 11 (Buck and Finn 2001; Fehr et al. 2002; Shirley et al. 2004; Hood et al. 2006). The Chr 4 QTL has been the best characterized; the associated QTG appears to be Mpdz (multiple PDZ domain protein; Fehr et al. 2002; Shirley et al. 2004). Focusing on the consumption/preference phenotype, QTLs have been confirmed on Chr 2, 3, 4, and 9 (Belknap and Atkins 2001). Of these, the Chr 9 QTL has been best characterized; putative QTGs are Hyou1 (Orp150; hypoxia upregulated protein 1) and Scn4b (sodium channel subunit beta-4; Mulligan et al. 2006). The overlap of the two data-sets is on Chr 4; however, the
