Abstract: The contribution of an impaired astrocytic K+ regulation system to epileptic neuronal hyperexcitability has been increasingly recognized in the last decade. A defective K+ regulation leads to an elevated extracellular K+ concentration ([K+]o). When [K+]o reaches peaks of 10–12 mM, it is strongly associated with seizure initiation during hypersynchronous neuronal activities. On the other hand, reactive astrocytes during a seizure attack restrict influx of K+ across the membrane both passively and actively. In addition to decreased K+ buffering, aberrant Ca2+ signaling and declined glutamate transport have also been observed in astrogliosis in epileptic specimens, precipitating an increased neuronal discharge and induction of seizures. This review aims to provide an overview of experimental findings that implicated astrocytic modulation of extracellular K+ in the mechanism of epileptogenesis.

Key words: AQP4, Ca²⁺ signaling, cell volume, connexins, epilepsy, K+ buffering, miRNA, NKCC, pannexin, TBI