Despite the innate benefits of the body’s ability to initiate a stress response, chronic activation of the hypothalamic-pituitary-adrenal (HPA) axis has been demonstrated to result in debilitating neuropsychiatric disorders that comprise the most prevalent forms of disability worldwide. Notably, chronic stress has extensively been study to lead to depressive disorders however, the exact mechanism by which chronic stress leads to depressive disorders is not fully known. Of interest to me is the demonstrated impacted of chronic stress on neurosteroids. Neurosteroids are endogenously produced in the brain and act as positive allosteric modulators of GABAARs, which is thought to contribute to their antidepressive and anticonvulsant properties. Following chronic stress, circulating levels of neurosteroids such as alloprgenanalone, decline, yet it is not known: 1. By which mechanism does chronic stress impacts neurosteroids, 2. how neurosteroids may interact with glucocorticoids during the stress response, and 3. how these effects may contribute to behavioral deficits observed in depressive disorders. Utilizing an array of biochemical assays, chemogenic and Cas-9 approaches, in conjunction with in vivo and ex vivo electrophysiology my work aims to elucidate the role of endogenous neurosteroidogenesis in mediating deficits in emotional processing caused by chronic stress.