be rewarding since animals learn to lever press for carbachol infusions into the VTA (Ikemoto and Wise, 2002). Conversely, DA levels in the NAc decrease in response to the muscarinic antagonist, scopolamine, and the nicotinic antagonist, mecamylamine, when applied to the VTA (Lester et al., 2008). Electrical stimulation of LDTg changes DA efflux in the NAc in a distinctive three component pattern (Forster and Blaha, 2000). The third and longest component, which is the sustained increase in DA, is mediated via M5 receptors located in the VTA (Forster et al., 2002; Williams and Adinoff, 2008). Electrical activation of the LDTg cholinergic neurons fails to activate the third component in the NAc of M5 receptor-deficient (M5R-/-) mice. A recent study by Lester et al. (2010) supports the role of M5 receptors in mediating the enhancing effects of cocaine on NAc DA efflux evoked by electrical stimulations of the LDTg. Whereas IP injections of cocaine enhanced NAc DA efflux evoked by the electrical stimulations in the LDTg, they failed to do so when scopolamine was also injected into the VTA. In fact, even when DA efflux reached its peak it plummeted to baseline levels if scopolamine was injected into the VTA. Behavioral
