Overeating typically follow periods of energy deficit or is sustained by highly palatable foods even without metabolic demand. Inhibitory dopamine D1- receptor expressing medium spiny neurons (D1-MSNs) of the nucleus accumbens shell (NAcSh) project to the lateral hypothalamus (LH) to authorize feeding when inhibited. Whether plasticity at these synapses affects feeding remains unknown. Here, ex vivo electrophysiology recordings combined with optogenetics revealed that accumbal shell D1-MSN-to-LH transmission is depressed in circumstances where overeating is promoted. Endocannabinoid signalling is identified as the induction mechanism. Collectively, our study reveals a critical role for plasticity at NacSh D1-MSN-to-LH synapse in adaptive feeding control and suggest that hypoactivity of this pathway may underlie persistent overeating of unhealthy food, a major risk factor for developing obesity.