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. 2014:114:155-85.
doi: 10.1016/B978-0-12-418693-4.00007-8.

Mechanisms of ictogenesis

Thomas Blauwblomme  1 , Premysl Jiruska  2 , Gilles Huberfeld  3
Affiliations

Mechanisms of ictogenesis

Thomas Blauwblomme et al. Int Rev Neurobiol. 2014.

Abstract

Epilepsy is a paroxysmal condition characterized by repeated transient seizures separated by longer interictal periods. Ictogenesis describes the processes of transition from the interictal state to a seizure. The processes include a preictal state, with specific clinical signs and a distinct electrophysiology which may provide opportunities to anticipate, or even prevent, seizures. Biological mechanisms of ictogenesis remain poorly understood and may vary between conditions/syndromes. We review here ictogenic processes including the involvement of pyramidal cells, interneurons and astrocytes, GABAergic and glutamatergic signaling, and ionic perturbations. Our review suggests that specific excitatory influences at the transition to an ictal event include (1) GABA receptor activation with a neuronal Cl(-) load and (2) a transient increase in external K(+).

Keywords: Chloride; Epilepsy; GABAergic signaling; Ictogenesis; Interneurons; Potassium; Pyramidal cells.

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