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Mechanisms of ictogenesis
T. Blauwblomme, P. Jiruska, G. Huberfeld,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NT14489
MZ0
CEP - Centrální evidence projektů
- MeSH
- draslík metabolismus MeSH
- epilepsie etiologie patologie MeSH
- lidé MeSH
- mozek patologie MeSH
- neurony metabolismus patologie MeSH
- receptory GABA metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
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(+).
Clinical Neurophysiology Department CHU Pitié Salpêtrière APHP Paris France
INSERM U1129 Infantile Epilepsies and Brain Plasticity Paris France
Neurosurgery Unit Hopital Necker Enfants Malades APHP Paris France
Université Paris Descartes Paris France
Université Pierre et Marie Curie Paris France
University Paris Descartes PRES Sorbonne Paris Cité Paris France
Citace poskytuje Crossref.org
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- $a 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(+).
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- $a Jiruška, Přemysl, $u 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. $d 1976- $7 xx0037786
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