Leptin is an adipocyte-derived hormone which links peripheral metabolic state to central control of energy balance. In addition to its role in maintaining energy homeostasis, leptin affects motivation for food reward and nutrient choices by modulating the mesolimbic dopamine system. Although leptin directly reduces activity of ventral tegmental (VTA) dopamine neurons, most of these dopamine neurons do not project to the accumbens which is the dopamine projection implicated in driving food reward seeking. So how does leptin then reduce motivation for food reward? Leptin receptors (LepR) are also expressed in GABA neurons in the ventral tegmental area (VTA) and lateral hypothalamus (LH). There are still gaps in knowledge that we address here: 1) which leptin-receptor expressing neurons connect to the dopamine system, 2) how does leptin modulate their activity and 3) which of these neurons is implicated in regulating the motivation to obtain food reward. We used optogenetic-assisted circuit mapping approach to show cell-type specific effects of leptin on reward circuitry. We demonstrate functional connectivity between LepR-expressing neurons in the LH and VTA neurons as well as LepR-expressing GABA neurons in the VTA and DA neurons. Chemogenetic activation of LH neurons increased the motivation to press lever to obtain a sucrose reward likely by decreasing VTA GABAergic input onto VTA dopamine neurons. We also find that VTA GABA neurons expressing leptin receptors project onto VTA dopamine neurons. Activation of leptin receptor expressing neurons in the VTA using chemogenetics reduced the motivation to press lever for a sucrose reward in food-restricted mice. We conclude that leptin indirectly targets multiple inputs to the dopamine system to reduce food reward seeking.