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Interleukin‐1β contributes to the generation of experimental febrile seizures
Author(s) -
Dubé Celine,
Vezzani Annamaria,
Behrens Marga,
Bartfai Tamas,
Baram Tallie Z.
Publication year - 2005
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.20358
Subject(s) - epilepsy , proinflammatory cytokine , febrile seizure , cytokine , receptor , transgene , neuroscience , genetically modified mouse , immunology , biology , medicine , inflammation , genetics , gene
Fever can provoke “febrile” seizures (FS). Because complex FS may promote development of temporal lobe epilepsy, understanding their mechanisms is clinically important. Using an immature rodent model and transgenic technology, we examined the role of interleukin‐1β, (IL‐1β), a pyrogenic, proinflammatory cytokine, in FS. IL‐1β receptor–deficient mice were resistant to experimental FS. This resistance appeared independent of genetic background and was attributed to lack of IL‐1β signaling, because exogenous cytokine reduced seizure threshold in wild‐type but not receptor‐deficient mice independent of strain. In addition, high IL‐1β doses induced seizures only in IL‐1β receptor–expressing mice. These data indicate that IL‐1β signaling contributes critically to fever‐induced hyperexcitability underlying FS, constituting a potential target for their prevention. Ann Neurol 2005;57:152–155 An Erratum has been published for this article in Ann Neurol 57: 609, 2005 .