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Is Slack an intrinsic seizure terminator?
University of Otago, Dunedin, New Zealand.ORCID iD: 0000-0002-1904-5554
2013 (English)In: The Neuroscientist, ISSN 1073-8584, E-ISSN 1089-4098, Vol. 19, p. 248-254Article in journal (Refereed) Published
Abstract [en]

Understanding how epileptic seizures are initiated and propagated across large brain networks is difficult, but an even greater mystery is what makes them stop. Failure of spontaneous seizure termination leads to status epilepticus—a state of uninterrupted seizure activity that can cause death or permanent brain damage. Global factors, like changes in neuromodulators and ion concentrations, are likely to play major roles in spontaneous seizure cessation, but individual neurons also have intrinsic active ion currents that may contribute. The recently discovered gene Slack encodes a sodium-activated potassium channel that mediates a major proportion of the outward current in many neurons. Although given little attention, the current flowing through this channel may have properties consistent with a role in seizure termination.

Place, publisher, year, edition, pages
Sage Publications, 2013. Vol. 19, p. 248-254
Keywords [en]
sodium-activated potassium channel, seizure termination, epilepsy, electrophysiology, slow afterhyperpolarization
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:liu:diva-171567DOI: 10.1177/1073858412446311ISI: 000318860800008PubMedID: 22645110Scopus ID: 2-s2.0-84877767971OAI: oai:DiVA.org:liu-171567DiVA, id: diva2:1503233
Available from: 2020-11-23 Created: 2020-11-23 Last updated: 2020-11-30Bibliographically approved

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Igelström, Kajsa

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