In this project, I investigated the endogenous role of hindbrain ghrelin receptors in regulating feeding behavior. In order to test our hypothesis that the hindbrain ghrelin receptor, growth hormone secretagogue receptor 1a (GHSR1a), plays a physiological role in the hindbrain to increase food intake we [1] chronically knocked down GHSR1a in the NTS using an AAV shRNA and [2] acutely injected the endogenous GHSR1a antagonist LEAP-2 into the fourth (hindbrain) ventricle. Throughout the course of the experiment, we measured chow intake and body weight after injecting either ghrelin or CCK to determined whether chow intake was increased or decreased. We also measured baseline chow intake and body weight before the experiment ran, and light versus dark cycle intake to determine if the knock down virus affected when the rat subjects consumed their food. In addition, we conducted a follow up experiment involving LEAP-2, the endogenous GHSR1a antagonist. We injected varying amounts of LEAP-2 and subsequently measured chow intake and body weight. The goal of the project was to determine how the chronic NTS knock down of GHSR1a affected chow intake and body weight in different scenarios and determine how hindbrain injection of LEAP-2 affected chow intake and body weight.