Epilepsy patients frequently report stress as a trigger for seizures and studies have shown that epilepsy patients exhibit increased levels of corticosterone. While studies have linked stress and epilepsy, not much is known about the mechanism underlying this relationship. My project in the Maguire lab builds upon data previously generated from the lab. The Maguire group has recently found the seizures exhibited by mice treated with chemoconvulsants hyperactivate the hypothalamic-pituitary-adrenal (HPA) axis via activation of corticotropin releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) of the hypothalamus. In a mouse model displaying increased CRH activity, I am investigating the hypothesis that status epilepticus induced hyperactivation of the HPA axis exacerbates neuropathology associated with chronic epilepsy, alters neural network connection, and contributes to the co-morbid appearance of anxiety and depression typically found in epilepsy patients.