that OxoSQ affects M2/4 receptors on non-cholinergic neurons cannot be excluded. Previous work shows that locus coeruleus (LC) noradrenergic neurons interconnect heavily with LDTg neurons (Jones, 1991; Leonard et al., 1995). Interestingly, M2 receptors are present on postsynaptic noradrenergic neurons, and their stimulation results in depolarization of the noradrenergic neurons (Egan and North, 1985). Elevated LC noradrenergic discharge rates are strongly associated with increased arousal (Berridge, 2008). Thus, it is possible that LC activity was affected by OxoSQ through M2 heteroreceptors. It is possible that the mild increases in locomotor activity seen after OxoSQ injections in our animals are attributable to M2 heteroreceptor activation. However, even if other M2/4 heteroreceptors were activated by OxoSQ, we contend that in our study direct microinjection of OxoSQ into the LDTg likely activated M2 autoreceptors on cholinergic neurons and thus suppressed their firing. This suppression is hypothesized to be a central cause of the decreased lever pressing for either cocaine or food. OxoSQ did not decrease lever pressing because it induced depressive-like behaviors, as many cholinomimetics do when administered systemically (Williams and Adinoff, 2008). In fact, OxoSQ at the higher dose used, when injected in the LDTg, slightly increased the activity of animals during
