α7 KO mice have been widely studied to explore the role of this subunit in nicotine’s effects. Grabus et al. (2005) examined withdrawal after chronic oral nicotine administration in α7 KO mice by replacing nicotine solutions with water. Withdrawal-induced hyperalgesia was attenuated in α7 KO compared to wild-type mice, but there was no difference in other aspects of nicotine withdrawal, such as the somatic signs (paw tremors, backing, head shakes). Similarly, Jackson et al. (2008) found that mecamylamine (MEC)-precipitated nicotine withdrawal in α7 KO mice implanted with osmotic mini-pumps resulted in a loss of hyperalgesia. No differences in the somatic signs of withdrawal were observed between nicotine-dependent wild-type α7 KO mice compared to saline-treated wild-type and α7 KO mice. In contrast, using a nicotine withdrawal protocol similar to Jackson et al. (2008) mice lacking the α7 subunit exhibited decreases in 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
