This project offers a new conceptual and operational approach to understanding the cellular basis of seizure disorders. If a dysregulation in astrocytic Ca2+ signaling indeed proves causal in epileptogenesis – as our data strongly suggest – then the implications of this new perspective to pharmacotherapy could be profound. The often imprecise correlation of anti-epileptogenic activity with synaptic suppression would be better understood, allowing new emphasis on therapeutic strategies intended to screen for agents able to suppress astrocytic Ca2+ signaling and/or glutamate release.
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