In particular, studies of null mutant (“knock-out”, KO) mice, which lack the α3 and β4 subunits have shown differential behavioral responses to nicotine. Heterozygous α3 animals (i.e. mice which carry one copy of the gene) are resistant to nicotine-induced seizures and hypolocomotion, suggesting a possible role of this gene in central responses to nicotine. β4 KO mice also show reduced sensitivity to the effects of nicotine on seizure induction and locomotion (Salas et al. 2004a), but otherwise appear normal and do not show any symptoms of nicotine withdrawal (Salas et al. 2004b). In addition, the α3 and β4-containing receptors in the habenula-interperduncular nucleus have recently emerged as potential targets for smoking cessation strategies (see review by (De Biasi and Salas 2008). For example, although the commonly prescribed treatment for smoking cessation, Varenicline, is a partial agonist of α4β2* receptors, it is also a full agonist of α7 and a partial agonist of α3β4* receptors, which have been shown to display higher efficacy (maximal release) than α4β2* receptors (Mihalak et al. 2006). Moreover, the antidepressant Bupropion, which alters brain reward circuits
