Complex interactions of internal and external factors drive overeating which leads to increased body weight and obesity. In our modern food environment, energy dense foods are typically overconsumed because they are easily accessible and highly palatable. Preclinical models of obesity have begun to examine how diet induced obesity impacts synaptic plasticity in brain regions that guide decision making and motivated feeding behavior. The orbitofrontal cortex (OFC) can influence food intake decisions as it integrates sensory information with limbic, prelimbic, and basal ganglia regions. Rats with OFC lesions consume food regardless of the updated sensory features and motivational value of the outcome, in a habit-like fashion. Given that habit-like eating is associated with obesity, it is possible that access to an obesogenic diet can influence OFC synaptic function. The lateral orbitofrontal cortex (lOFC) consists of pyramidal output neurons arranged in layers along with inhibitory GABAergic interneurons and astrocytes. Diet induced obesity alters inhibitory signaling, along with morphological changes in pyramidal neurons and astrocytes. However how pyramidal neuron disinhibition influences lOFC neuronal activity and behavior is unknown. Furthermore, how pyramidal neurons in the lOFC respond acutely to high-fat caloric dense food leading to the etiology of diet induced obesity has yet to be elucidated. Chapter 1 critically evaluates and reviews literature describing the functionality of the OFC, and the neurobiology and corresponding behaviours on the effects of a high-fat diet leading to obesity. Chapter 2 examines how diet-induced obesity disinhibits pyramidal neurons in the lOFC and biases decision making. In Chapter 3 how lOFC pyramidal neurons respond to energy status is examined, our results indicate that short- and long- term high-fat diet exposure differentially alters GABAergic signalling in the lOFC. This thesis provides insight on how consumption of a high-fat diet alters the lOFC; a brain region involved in the self-regulation of food intake. This has implications in present society as palatable caloric-dense foods are abundantly available and chronic consumption can lead to weight gain, diet induced obesity and comorbid health conditions.