We seek to understand the mechanisms by which heterogenous cell types orchestrate synchronous network patterns for brain computations as fundamental as memory, which may be key to understanding the origins of pathological hypersynchrony in epilepsy. Using cutting-edge in vivo approaches (e.g., 2-photon imaging and single cell optogenetics, high density electrophysiology, genetically encoded biosensors) to home in on these mechanisms with precision, our goal is to restore circuit function with minimal side effects. As a step towards translation, we are developing new tools to uncover mechanisms of ultrasound neuromodulation and use parameter-optimized stimulation patterns to achieve cell type-specificity, but without the need for surgery or genetic manipulations.

Another project in the lab pertains to the organization of endocannabinoid signaling in the brain, which relies on the brain’s most abundant GPCR, the CB1 receptor. We use 2-photon imaging and genetically-encoded biosensors to study the dynamics of this system in awake behaving mice. We are interested in how the endogenously synthesized ligand for this receptor, 2-AG, can potently regulate activity at synapses, but also provide substrate for neuroinflammatory lipids. Thus, this signaling system can have opposing roles in pathophysiology and is a prime target for intervention.