the somatic signs of MEC-precipitated withdrawal and exhibited normal MLA-precip-itated nicotine withdrawal, compared to wild-type mice (Salas et al. 2007). The opposing results from Jackson et al. (2008) and Salas et al. (2007) indicate a clearly undefined role of the α7 subunit in nicotine withdrawal, suggesting the possibility that there may be α7* nACh receptors that assemble with other subunits (Khiroug et al. 2002; Palma et al. 1999) that respond differently to the nAChR antagonists used to precipitate withdrawal. MEC is highly selective for α3β4* nAChRs, has a very low affinity for α7 nAChRs (Papke et al. 2001), and has been shown to be the most effective nAChR antagonist at precipitating both the somatic and non-somatic signs of withdrawal (Damaj et al. 2003; David et al. 2007; Malin et al. 1998). MLA, however, is a selective antagonist for α7 nAChRs (Roegge and Levin 2006) and has demonstrated contrasting results in nicotine withdrawal. MLA did not induce somatic signs of withdrawal after prolonged nicotine exposure in rats (Markou and Paterson 2001), but consistent with Salas et al. (2007), Damaj et al. (2003) showed that MLA was able to precipitate withdrawal, suggesting that MLA may have specificity for nAChR subunits other than
