In contrast to the increased firing rate of cholinergic neurons in the PPTg in response to contextual information related to reward, tonically active cholinergic interneurons in the striatum pause their firing following exposure to cues associated with reward (Goldberg and Reynolds, 2011). The pause is thought to be mediated by interactions between the cells’ intrinsic membrane properties and strong feed-forward excitation from the thalamus (Ding et al., 2010). These cholinergic interneurons can regulate the duration, magnitude, and spatial pattern of activity of striatal neurons, potentially creating an attentional gate that facilitates movement toward salient stimuli (Oldenburg and Ding, 2011). Function of striatal cholinergic interneurons is also impaired in patients with movement disorders that are dependent on function of the dopaminergic system such as Parkinson’s and Huntington’s disease and in animal models of these diseases (Ding et al., 2011). Cholinergic signaling in striatum and NAc is also thought to be critical for mediating the association between drugs of abuse and cues in the environment that drive drug craving and relapse to drug use after abstinence (Exley and Cragg, 2008). The effects
