Obesity is driven and maintained by dysregulation of appetite. Especially nowadays, with rich availability of palatable processed food, overeating promotes weight gain through unbalancing energy expenditure and intake. Lifestyle interventions are foundation of obesity management; however, the long-term maintenance is challenging. Thus, understanding the neural mechanism underlying compulsive overeating is urgent for better weight control. Dopamine system and hypothalamus are highly involved in obesity, proved by fMRI in patients. In mice, our lab discovered that a specific subset of nucleus accumbens (NAc) D1-MSNs projecting to the lateral hypothalamus (LH) authorizes feeding. As the potentiation of NAc D1-MSNs is responsible for cocaine induced adaptive behavior, we hypothesize that plasticity on NAc LH-projectors could be also necessary for the long-term weight increase in compulsive overeating. Here, we first observed decreased excitatory transmission on NAc LH-projectors acutely after food restriction by ex vivo electrophysiological recordings. To clarify which are the major inputs contributing to that, we performed TRIO experiment and located PVT, BLA, Xi and vHipp. Combining retrograde tagging and optogenetics in patch clamp experiments, we found reduced AMPA/NMDA on NAc LH-projectors receiving afferents from vHipp. Further, we constructed an in-cage intermittent compulsive feeding paradigm with consumption monitored automatically, and explored the plasticity on NAc LH-projectors after long-term exposure as well as abstinence to highly palatable food. We also assessed neuronal activity change during the building process of compulsive overeating. We would like to address the interaction between plasticity and compulsive overeating, to develop better management methods for obesity.