Relatively low concentrations of insulin produce increased glutamate release in the NAc and enhance dopamine release in this region through actions on cholinergic interneurons. As insulin concentrations increase, activation of IGFRs is recruited, causing a reduction in glutamate release. In addition, at these higher concentrations, local dopamine release within the NAc is no longer enhanced, and instead insulin results in LTD of VTA-dopamine neurons. Thus, small anticipatory increases in insulin in response to stimuli associated with food may activate local NAc circuits to promote food pursuit, while larger post-prandial increases in insulin may reduce activity in the VTA and NAc to reduce the pursuit of food and promote feeding cessation.