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Midbrain dopaminergic neurons (DA) are thought to con-vey information about the rewarding or motivationallyrelevant properties of external stimuli. Furthermore, evi-dence has accumulated that dopamine signaling isinvolved in the rewarding and aversive motivational prop-erties of drugs of abuse, including nicotine. DA neuronsproject from the ventral tegmental area (VTA) to variousstructures including the nucleus accumbens (NAcc) andthe prefrontal cortex. Like other drugs of abuse, nicotineincreases dopamine levels in the NAcc. While nicotinicacetylcholine receptors (nAChRs) are expressed through-out the central nervous system, this increase has beendemonstrated to result from a direct stimulation ofnAChRs in the VTA [1]. Nicotine concentrations reachedduring smoking activate and subsequently desensitizenAChRs. However, the mechanism of how the dopamin-ergic signal in response to nicotine exposure is con-structed in the VTA remains elusive. Especially,

Nicotine and the dopaminergic output of the ventral tegmental area