Overconsumption of highly palatable ‘junk’ foods is a primary contributor to the development of obesity. There is increasing evidence that the pathological overeating which often underlies obesity is compulsive in nature and therefore contains elements of an addictive disorder. However, direct physiological evidence linking obesity to synaptic plasticity akin to that occurring in addiction is lacking. We have accumulated evidence using a rat model of diet-induced obesity which suggests that the propensity to diet-induced obesity is associated with addiction-like behavior and hallmark synaptic impairments in the glutamatergic input to the nucleus accumbens core (NAcore) previously observed in rodent models of drug addiction. Diet-induced obese and resistant rats were assessed for operant self-administration of palatable food pellets using fixed and progressive ratios in order to determine whether they would display features of ‘addiction-like’ behavior towards palatable food – heightened motivation as assessed by progressive ratio, excessive intake, and the persistence of responding during periods where pellets were unavailable. Subsequently, NAcore brain slices were prepared and we tested for changes in the ratio between AMPA and NMDA currents (AMPA/NMDA) and the ability to exhibit long-term depression (LTD). Obesity prone rats were more ‘food addiction’ vulnerable than their obesity resistant counterparts as displayed by i) heightened motivation ii) excessive consumption and ii) increased food-seeking as measured by lever-pressing during periods where palatable food was unavailable. Moreover, rats prone to diet-induced obesity exhibited deficits in the ability to induce LTD in the nucleus accumbens core as well as increased potentiation at these synapses as measured by the ratio of AMPA/NMDA currents. These are hallmark synaptic impairments that have been observed in the brains of animals that have self-administered drugs of abuse such as cocaine, nicotine and heroin. Our results show overlap between the propensity to obesity and synaptic changes associated with drug addiction, supporting partial coincident neurological underpinnings for obesity and drug addiction.