CHARACTERIZING NEUROVASCULAR INTERACTIONS DURING EPILEPTIC SEIZURES IN ZEBRAFISH

Zebrafish larvae have become a powerful vertebrate model for studying seizures and epilepsy, offering unparalleled advantages such as genetic accessibility, rapid development, and optical transparency that enable non-invasive, whole-brain imaging of neural and glial activity at cellular resolution. Despite growing insights into neuronal and glial dynamics during epileptic events, the interplay between these networks and the cerebrovascular system, particularly the mechanisms of neurovascular coupling during seizures, remains poorly understood. This gap is critical, as vascular dysfunction and blood–brain barrier (BBB) breakdown are increasingly recognized as contributors to epileptogenesis and seizure propagation by intensifying network instability and sustain/exacerbate seizure activity. This project aims to systematically characterize spatiotemporal alterations in neurovascular coupling across distinct phases of pentylenetetrazole (PTZ)-induced seizure activity in zebrafish. Using multi-channel confocal imaging combined with high-speed blood flow measurements, we simultaneously monitor vascular architecture, hemodynamic parameters, and BBB integrity alongside neural and glial calcium dynamics. This integrated approach allows us to capture real-time interactions between vascular and neural compartments during both acute seizures and chronic epileptic states. Our preliminary findings reveal region-specific vascular remodeling and heterogeneous changes in blood flow during seizures, accompanied by disruptions in BBB permeability. These observations suggest that impaired neurovascular coupling induces spatially restricted alterations in vascular dynamics, creating region-specific vulnerabilities that modulate both the susceptibility of distinct neural circuits to seizure propagation and the evolving trajectory of epileptic activity.We are currently comparing acute and chronic PTZ models to identify conserved patterns of neurovascular dysfunction and to map their temporal progression during epileptogenesis.