title: Mechanisms of ictogenesis.
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(+).
authors: Neurosurgery Unit, Hopital Necker-Enfants Malades, APHP, Paris, France; Université Paris Descartes, Paris, France; INSERM U1129-Infantile Epilepsies and Brain Plasticity, Paris, France; University Paris Descartes, PRES Sorbonne Paris Cité, Paris, France; CEA, Gif sur Yvette, France.
authors: Thomas
authors: T
authors: Blauwblomme
authors: Department of Developmental Epileptology, Institute of Physiology, Academy of Sciences of Czech Republic, Prague, Czech Republic; Department of Neurology, 2nd Faculty of Medicine, Charles University in Prague, Motol University Hospital, Prague, Czech Republic.
authors: Premysl
authors: P
authors: Jiruska
authors: INSERM U1129-Infantile Epilepsies and Brain Plasticity, Paris, France; University Paris Descartes, PRES Sorbonne Paris Cité, Paris, France; CEA, Gif sur Yvette, France; Clinical Neurophysiology Department, CHU Pitié-Salpêtrière, APHP, Paris, France; Université Pierre et Marie Curie, Paris, France. Electronic address: gilles.huberfeld@upmc.fr.
authors: Gilles
authors: G
authors: Huberfeld
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology; D004827:Epilepsy / Q000209:etiology* / Q000473:pathology*; D006801:Humans; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D011188:Potassium / Q000378:metabolism; D018079:Receptors, GABA / Q000378:metabolism*
chemical_list: D018079:Receptors, GABA; D011188:Potassium
keywords: Chloride; Epilepsy; GABAergic signaling; Ictogenesis; Interneurons; Potassium; Pyramidal cells