At the cellular level, stimulation of nAChRs and mAChRs on lateral hypothalamic (LH) neurons increases and decreases GABA release, respectively (Jo and Role, 2002). The data suggest that the nAChRs and mAChRs may be localized to different populations of GABAergic terminals, but from these studies it is difficult to determine what the effects of synaptically evoked ACh on LH GABA release might be. Optogenetic stimulation of cholinergic transmission in the LH and hypothalamus will be useful in identifying the source of ACh input to these areas, the role of intrinsic ACh in hypothalamic function, and the differential role of mAChRs and nAChRs in shaping responses to ACh in these brain regions. In the arcuate nucleus of the hypothalamus, nicotine increases the firing rate of both POMC- and neuropeptide Y (NPY)-positive neurons, although the increase in POMC neuron activity predominates in vitro due to more rapid desensitization of nAChR responses in NPY neurons, and in vivo, as evidenced by an increase in c-fos immunoreactivity predominantly in POMC-positive cells (Huang et al., 2011; Mineur et al., 2011). Thus, as in the mesolimbic
