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Elucidating the Involvement of Endothelial TRPC3 Channels in Neurovascular Coupling During Status Epilepticus

Neurovascular coupling is the relationship between local neural activity and resulting changes to blood flow. In a non‐pathological state, local increases in neural activity result in greater metabolic needs which are then satisfied by increased blood flow to the region. As neural activity increases greatly during Status Epilepticus (SE), a commensurate increase in blood flow is also expected. However, we have observed an inverse hemodynamic response at the onset of seizure activity which evidences SE‐induced dysregulation of normal neurovascular coupling. Canonical transient receptor potential channel 3 (TRPC3) is a cation channel that regulates intracellular calcium. Our previous results confirmed its contribution to both physical manifestations of seizure and neural seizure activity in a pilocarpine model of SE. Current literature suggests that TRPC3 channels expressed specifically in cerebrovascular endothelial cells are involved in the regulation of neurovascular coupling and contribute to vasodilation, therefore they may also be involved in its dysregulation during epileptogenesis. In this study, we investigate the precise role of endothelial cell TRPC3 channels in neurovascular coupling during SE.