PROJECT SUMMARY Obesity and diabetes are an epidemic in the United States with more than third of US adults now defined as obese. Some of the most effective therapies to manage glucose homeostasis and weight target the glucagon- like peptide 1 receptor (GLP-1R). Many studies demonstrate that systemic GLP-1R agonists produce changes in appetite and hypophagia through the activation of GLP-1Rs in the brain, where their expression is widespread. Recent efforts to characterize the role of GLP-1Rs in specific brain nuclei and circuits have mainly focused on the hypothalamus and hindbrain, whereas the function of GLP-1Rs in limbic systems like the amygdala have received less attention and study. The amygdala, the brain’s emotional processing core, is well known for its role in fear and anxiety, but recent data from our lab and others have demonstrated a clear role for positive valence, promoting appetitive food-seeking behavior, and driving food intake. In a recent publication, our lab described the expression of GLP-1Rs in the central subnucleus of the amygdala (CeA) and characterized the neural physiology of GLP-1R-expressing neurons. In this fellowship, we will pursue a functional analysis of 1) GLP-1Rs on the control of neural activity in the CeA and 2) determine the requisite role of CeA neural activity-changes on the hypophagic actions of peripherally administered GLP-1R agonists. Our studies will have important implications for understanding the cellular and molecular mechanism of action of now widely prescribed obesity and type II diabetes therapeutics.