α6-containing nAChRs are expressed mainly in brain areas that are involved in nicotine-stimulated dopamine release (Champtiaux et al. 2003; Lai et al. 2005; Salminen et al. 2004), and have been implicated in mediating nicotine dependence (Laviolette and van der Kooy 2004). One of the first studies examining the pharmacology of α6-containing nAChRs generated mice lacking the α6 subunit gene (Champtiaux et al. 2002). Null mutant mice had no high-affinity α-conotoxin MII-sensitive (α6 selective antagonist) binding sites (Champtiaux et al. 2002; Drenan et al. 2008; Yang et al. 2009). A majority of β3 subunits are assembled with α6 subunits (Champtiaux et al. 2003; Yang et al. 2009) and chronic nicotine treatment decreases α6-containing nAChRs in the striatum but does not change the density of α6 nAChRs that contain β3 subunits (Perry et al. 2007). Jackson and others measured physical (somatic and hyperalgesia) and affective [anxiety-related behavior and conditioned place aversion (CPA)] nicotine withdrawal behaviors in C57BL/6J mice implanted with osmotic mini-pumps filled with nicotine or saline for 14 days (28 days for CPA). Withdrawal was initiated after 14 days of nicotine
