Overeating leading to obesity is highly influenced by non-homeostatic or hedonic signals to the brain circuit underlying motivation for food, especially in an environment where highly caloric, palatable foods are easily accessible. A circuit underlying motivation to consume food includes dopamine neurons of the ventral tegmental area (VTA) and their axon terminals in the ventral striatum. These neurons are a target for many peripheral signals relaying hunger or satiety information.  Our previous work has demonstrated that insulin can suppress excitatory synaptic transmission onto dopamine neurons via an endocannabinoid-mediated mechanism. Additionally, insulin administered to the VTA can decrease dopamine release in the nucleus accumbens, as well as reduce hedonic feeding or conditioned place preference for palatable food.  One or 24 hour access to palatable food induces an endocannabinoid-mediated synaptic depression. However, with 24 hour access to palatable food, the synaptic depression was offset by an increase in glutamatergic synaptic density onto dopamine neurons. This was followed days later by an increase in glutamatergic synaptic strength that lasted at least a week.  Furthermore, latencies to exit a dark box to an illuminated area containing palatable food was decreased in mice 48 hours after short-term access to palatable food. After the behavioural test, mice given short-term access to palatable food consumed more food that mice pre-exposed to a just a pellet of the food. These effects were blocked by intra-VTA insulin, a treatment known to reduce excitatory synaptic efficacy onto dopamine neurons.  Taken together, short-term access to palatable food can cause a long-lasting increase of synaptic efficacy onto dopamine neurons and promote future food seeking.