Our lab is one of the few that possesses the expertise, cutting-edge techniques, and animal model necessary to thoroughly answer important questions regarding cellular mechanisms underlying brain network excitability, such as epilepsy and spreading depolarization (SD), both of which are seen after traumatic brain injury (TBI) and associated with worsened clinical outcomes.

Traumatic brain injury (TBI) persists as the leading cause of death among young and elderly populations despite massive advancements in medical care, which is why the primary objective of my laboratory is to understand the mechanisms responsible for network disruptions underlying traumatic brain injury. TBI survivors are often profoundly affected by long-term increases in brain excitability; however, the slow progression from acute injury to chronic brain dysfunction presents an opportunity to examine the mechanisms beneath these brain changes. We use the mouse traumatic brain injury model to ask how the dynamics of cellular intrinsic mechanisms process incoming synaptic information to influence network behavior during the critical hours and days following brain injury. As a primary tool we use single cell recordings with whole-cell patch electrophysiological technique to analyze cells' membrane properties and synaptic transmission, and use two-photon imaging in the awake behaving animal to measure presynaptic excitatory glutamate transmission and post-synaptic calcium changes, with the goal of dissecting how particular neural circuits affected by brain injury.