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It has been postulated that glia play a critical role in modifying neuronal activity,mediating neurovascular coupling, and in seizure initiation. We investigated the role ofglia in ictogenesis and neurovascular coupling through wide-field multicell and 2-photonsingle cell imaging of calcium and intrinsic signal imaging of cerebral blood volume in anin vivo rat model of focal neocortical seizures. Ictal events triggered a slowlypropagating glial calcium wave that was markedly delayed after both neuronal andhemodynamic onset. Glial calcium waves exhibited a stereotypical spread that terminatedprior to seizure offset and propagated to an area ~60% greater than the propagation areaof neural and vascular signals. Complete blockage of glial activity with fluoroacetateresulted in no change in either neuronal or hemodynamic activity. These ictal glial waveswere blocked by carbenoxolone, a gap junction blocker. Our in vivo data reveal that ictalevents trigger a slowly propagating, stereotypical glial calcium wave, mediated by gapjunctions, that is spatially and temporally independent of neuronal and hemodynamicactivities. We introduce a novel ictally triggered propagating glial calcium wave callinginto question the criticality of glial calcium wave in both ictal onset and neurovascularcoupling.

Glial Calcium Waves are Triggered by Seizure Activity and Not Essential for Initiating Ictal Onset or Neurovascular Coupling