Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6266701 | Current Opinion in Neurobiology | 2014 | 8 Pages |
Abstract
Concepts of epilepsy, based on a simple change in neuronal excitation/inhibition balance, have subsided in face of recent insights into the large diversity and context-dependence of signaling mechanisms at the molecular, cellular and neuronal network level. GABAergic transmission exerts both seizure-suppressing and seizure-promoting actions. These two roles are prone to short-term and long-term alterations, evident both during epileptogenesis and during individual epileptiform events. The driving force of GABAergic currents is controlled by ion-regulatory molecules such as the neuronal K-Cl cotransporter KCC2 and cytosolic carbonic anhydrases. Accumulating evidence suggests that neuronal ion regulation is highly plastic, thereby contributing to the multiple roles ascribed to GABAergic signaling during epileptogenesis and epilepsy.
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Authors
Kai Kaila, Eva Ruusuvuori, Patricia Seja, Juha Voipio, Martin Puskarjov,