- BSc, Biology, American University, Washington, DC
- PhD, Developmental & Cellular Biology, George Washington University, Washington, DC
The main goal of my research is to understand how synaptic inhibition in the CNS is controlled by factors that regulate chloride homeostasis, and whether those factors can be targeted for therapeutic intervention. The major mediator of synaptic inhibition in the CNS is the GABAA receptor, which is also the target of numerous widely used medications such as Xanax, Ambien, and Valium. But what is less well known is that GABAA signaling is itself strongly controlled by another factor called KCC2, which pumps chloride out of neurons. Unfortunately, KCC2 function is impaired in many neurological disorders. This KCC2 dysfunction impairs both inhibitory synaptic transmission mediated by GABAA receptors as well as the effects of the widely used medicines that target those receptors. I have focused primarily on KCC2 dysfunction in seizure-related disorders, using the gold standard patch-clamp and electrophysiological techniques to carry out experiments. Combining unique genetic and pharmacological tools, we strive to improve the health of those who need our help.