There is a well-supported role of nicotine as the pharmacological agent that maintains dependence. The composition, anatomical localization, and physiological properties of nAChRs contribute to various physiological and behavioral differences (Govind et al. 2009; Marks et al. 1999). Nicotine and other nicotine agonists will elicit different responses of these receptors depending on the subtype it acts on (Brioni et al. 1997; Changeux 2010; Govind et al. 2009). Nicotine stimulates release of dopamine in the mesoaccumbens reward pathway (Champtiaux et al. 2003) and dependence is mediated, in part, by activation of specific subtypes of nAChRs on dopamine neurons (Court et al. 1998; Picciotto and Corrigall 2002). Dopamine release signals a pleasurable experience and is a key component of the reinforcing effects of nicotine and other drugs of abuse (Changeux 2010; Nestler 2005). Via nAChRs, nicotine activates both dopamine and GABA neurons of the ventral tegmental area (VTA), resulting in dopamine release in the nucleus accumbens and contributing to the rewarding and motivational effects of nicotine (Corrigall et al. 1994; Laviolette and van der Kooy 2004; Mineur and Picciotto 2008; Nisell et
