The adiposity hormone leptin is a critical modulator of energy balance. Apart from its hypothalamic actions, leptin regulates neural circuits controlling reward, motivation and emotion. Leptin has been shown to inhibit motivated behavior for rewarding electrical brain stimulation and palatable food. Dopamine (DA) neurons of the midbrain ventral tegmental area (VTA) are an essential component of the neural circuitry regulating motivation and reward. Via the long-form of its receptor (LepRb) leptin targets the VTA to inhibit feeding, food-motivated behavior, locomotion, and anxiety. Stat3 is the predominant signal whereby leptin regulates gene expression and leptin induces Stat3 phosphorylation in dopamine (DA) and GABA neurons of the VTA. We generated DA-specific Stat3 knockout (KO) mice to determine the contribution of LepRb-Stat3 signaling in midbrain DA neurons. While showing a similar anorectic response to leptin, KO mice exhibit marked impairments in food-motivated operant learning. In addition to large increases in ambulatory activity and voluntary running in male KO mice, the rewarding aftereffects of running are significantly elevated. These behavioral changes are accompanied by decreases in DA biosynthesis and D1 receptor protein expression in the nucleus accumbens. Our findings suggest an important role for leptin in attenuating running reward that are mediated via LepRb-Stat3 signaling in midbrain DA neurons and changes in DA tone. We posit that leptin acts in mesolimbic brain reward circuitry as a signal-of-plenty to dampen the motivational and rewarding effects of several behaviors that serve to replenish energy stores.