Astrocyte calcium signaling and epilepsy

AbstractStudies performed over the last decade, in both animal models and human epilepsy, support the view that a defective K+ buffering due to an altered expression of K+ and aquaporin channels in astrocytes represents a possible causative factor of the pathological neuronal hyperexcitability in the epileptic brain. More recent studies, however, reappraised the role of neurons in epileptogenesis and suggested that Ca2+?dependent gliotransmission directly contributes to the excessive neuronal synchronization that predisposes the brain network to seizures. Significant support for this view comes from the finding that astrocytes from hyperexcitable networks respond to neuronal signals with massive Ca2+ elevations and generate a recurrent excitatory loop with neurons that has the potential ...

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