title: Epileptogenesis in experimental models.
abstract: Epileptogenesis refers to a phenomenon in which the brain undergoes molecular and cellular alterations after a brain-damaging insult, which increase its excitability and eventually lead to the occurrence of recurrent spontaneous seizures. Common epileptogenic factors include traumatic brain injury (TBI), stroke, and cerebral infections. Only a subpopulation of patients with any of these brain insults, however, will develop epilepsy. Thus, there are two great challenges: (1) identifying patients at risk, and (2) preventing and/or modifying the epileptogenic process. Target identification for antiepileptogenic treatments is difficult in humans because patients undergoing epileptogenesis cannot currently be identified. Animal models of epileptogenesis are therefore necessary for scientific progress. Recent advances in the development of experimental models of epileptogenesis have provided tools to investigate the molecular and cellular alterations and their temporal appearance, as well as the epilepsy phenotype after various clinically relevant epileptogenic etiologies, including TBI and stroke. Studying these models will lead to answers to critical questions such as: Do the molecular mechanisms of epileptogenesis depend on the etiology? Is the spectrum of network alterations during epileptogenesis the same after various clinically relevant etiologies? Is the temporal progression of epileptogenesis similar? Work is ongoing, and answers to these questions will facilitate the identification of molecular targets for antiepileptogenic treatments, the design of treatment paradigms, and the determination of whether data from one etiology can be extrapolated to another.
authors.affiliation: Department of Neurobiology, A.I. Virtanen Institute for Molecular Sciences, University of Kuopio, Kuopio, Finland. Asla.Pitkanen@uku.fi
authors.forename: Asla
authors.initials: A
authors.lastname: Pitkänen
authors.forename: Irina
authors.initials: I
authors.lastname: Kharatishvili
authors.forename: Heli
authors.initials: H
authors.lastname: Karhunen
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Lukasiuk
authors.forename: Riikka
authors.initials: R
authors.lastname: Immonen
authors.forename: Jaak
authors.initials: J
authors.lastname: Nairismägi
authors.forename: Olli
authors.initials: O
authors.lastname: Gröhn
authors.forename: Jari
authors.initials: J
authors.lastname: Nissinen
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004569:Electroencephalography / Q000706:statistics & numerical data; D004827:Epilepsy / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D005544:Forecasting; D015870:Gene Expression; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D008967:Molecular Biology; D009410:Nerve Degeneration / Q000473:pathology / Q000503:physiopathology; D010641:Phenotype; D051381:Rats; D012107:Research Design / Q000639:trends; D012640:Seizures / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D020521:Stroke / Q000473:pathology / Q000503:physiopathology; D014743:Videotape Recording
chemical_list: D007473:Ion Channels