Epilepsy

Our epilepsy research focuses on how chloride cotransporters, particularly NKCC1, drive the hyperexcitability that underlies chronic epilepsy. Using a pilocarpine-induced rat model of temporal lobe epilepsy, we combine in vitro hippocampal electrophysiology with EEG recordings to characterize how altered chloride dynamics compromise GABAergic inhibition in dentate gyrus granule cells and the axon initial segment of pyramidal neurons — a site we've shown plays a distinct role in controlling neuronal excitability.

This mechanistic work has directly informed translational studies, including our work showing that bumetanide, an NKCC1 inhibitor, enhances the antiepileptic effect of conventional drugs like phenobarbital, and more recent work evaluating c-Abl inhibition as a way to reduce neuronal damage and seizure severity.