Mechanisms of ictogenesis
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
25078502
DOI
10.1016/b978-0-12-418693-4.00007-8
PII: B978-0-12-418693-4.00007-8
Knihovny.cz E-resources
- Keywords
- Chloride, Epilepsy, GABAergic signaling, Ictogenesis, Interneurons, Potassium, Pyramidal cells,
- MeSH
- Potassium metabolism MeSH
- Epilepsy etiology pathology MeSH
- Humans MeSH
- Brain pathology MeSH
- Neurons metabolism pathology MeSH
- Receptors, GABA metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Potassium MeSH
- Receptors, GABA 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(+).
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