Following a stressful event, the Hypothalamus - Anterior Pituitary - Adrenal (HPA) axis mediates the release of the stress hormone cortisol (corticosterone in rodents) (CORT). This CORT response serves to liberate energy and overcome stressors by binding to glucocorticoid receptors (GR); additionally, previous studies have demonstrated it has a modulatory role in memory formation. Under conditions of chronic stress, the release of CORT can be sensitized leading to an increased CORT response to fear conditioning. Rodents exposed to chronic stress demonstrate the formation of enhanced contextual fear memories, and previous research has shown that the basolateral amygdala (BLA) is a key brain region in the formation of contextual memories. It is currently unknown if the chronic stress enhancement of fear memory is caused by the sensitization of the CORT response. It is hypothesized that CORT is necessary for the chronic stress induced enhancement of fear memory. Therefore, GR antagonist, RU38486, was administered into the BLA 30 minutes prior to fear conditioning. Rats were separated into four treatment groups: chronic stress + GR-antagonist, chronic stress + saline, control + GR-antagonist, and control + saline. Following 2-3 weeks recovery post-surgery, rats in the chronic stress groups were subjected to a 4 day mild chronic stress paradigm that concluded with fear conditioning; 24 hours later rats were returned to the operant box and assessed for freezing behavior. Results are currently pending. Future studies based off collected data will indicate where further investigation of CORT’s role will be directed.