Dopamine (DA) transmission is associated with the reinforcement of goal-directed behavior acquired through trials and errors and its dysfunction leads to the pathogenesis of anhedonia and amotivation that are shared by several psychiatric disorders. Based on the previous studies of addiction, we developed a new reinforcement schedule of the instrumental lever-pressing for natural reward (food) in rats that allows us to evaluate two reinforcement-related parameters, "hedonic set point" and "demand elasticity," which are proportional to the inverse of the reward- and motivational effects, respectively. To investigate the role of the ventral tegmental area (VTA) DA neurons in the regulation of these parameters, we employed ionotropic chemogenetic tools: the IR84a/IR8a complex, a phenylacetic acid (PhAc) receptor of D. melanogaster, to activate the target neurons reversibly, and ivermectin (IVM)-gated chloride channel (GluCl) derived from C. elegans to reversibly inhibit the activity of the target neurons. We induced an expression of the IR84a/IR8a complex or GluCl in the VTA DA neurons using a Cre-loxP system in transgenic rats (Drd2-Cre rats). When we induced a PhAc-evoked activation in the IR84a/IR8a expressing VTA DA neurons, significant elevations in the extracellular DA level were found in the nucleus accumbens (NAc) core and dorsomedial striatum (DMS) but not in the NAc shell, suggesting that the NAc core and DMS are the functional terminals of the VTA DA neurons. Then, we examined the behavioral effects of the DA projection inhibition. An IVM systemic administration and microinjection into the NAc core significantly increased demand elasticity and hedonic set point. IVM microinjection into the VTA increased only demand elasticity. These results illustrate the multidimensionality of the reinforcement and the complex role of the DA projection system supporting its elements and suggest a complicated mechanism to modulate the reward effect through the NAc core.