Glucagon-like peptide 1 (GLP-1) is produced in the intestine and in neurons of the caudal brainstem, and GLP-1 can act at distinct sites in the periphery and in the brain to affect food intake. Recent studies in our laboratory have focused on the role of GLP-1 neurons in the control of feeding in the rat. Hindbrain GLP-1 neurons project to many brain areas known to be involved in the control of energy balance. One of these projection sites is the Nucleus Accumbens (NAc), known for its role in reward and motivated behavior. We characterized this projection using retrograde neuronal tracers injected into the NAc combined with immunofluroescent histochemical staining for GLP-1 in the caudal brainstem. In a series of studies, we examined rats' behavioral responses to direct injection of GLP-1 or GLP-1R antagonist into the NAc. Stimulation of GLP-1 receptors (GLP-1R) in the NAc Core, but not the Shell, suppressed chow intake for up to 24 h after an acute treatment.Blockade of GLP-1R in the NAc Core increased food intake, providing strong support for the hypothesis that endogenous GLP-1 release at this site contributes to physiologic control of feeding. Ongoing research is focused on the mechanisms through which NAc GLP-1R activity affects food intake. These studies identify a novel site for endogenous central GLP-1 action and raise the possibility that exogenous pharmacologic GLP-1R agonist treatments exert their anorexic effects in part by acting in the NAc.