My dissertation project at Emory University involved investigating the role of stress in a genetically predisposed epilepsy model. The Escayg lab uses mice with various mutations in voltage-gated sodium channels to understand the mechanisms of epilepsy. My work focused on two lines of mice, one with a missense mutation in the voltage-gated sodium channel gene Scn1a and one with a null mutation in the voltage-gated sodium channel gene Scn8a. In particular, I investigated how acute stress and early life stress affected seizure outcome. Previous work examining how stress can affect seizure outcome had been performed in wildtype animals with normal brain and stress system development. I have shown that having an "epileptic" brain is sufficient to alter the stress response, indicating the need for new research into how stress actually affects the epileptic brain. The ultimate goal is to find new therapeutic targets for the treatment of epilepsy.
I used a variety of techniques in my research including, but not limited to: EEG surgery in mice, EEG signal collection, EEG analysis, PCR, real-time PCR, behavioral assays and analysis, stress inducement (acute, chronic, and early life), blood collection in mice, radioimmunoassays, perfusions, immunohistochemistry, various seizure induction paradigms, mouse colony maintenance.