Interleukin-1β contributes to the generation of experimental febrile seizures

Celine Dubé, Annamaria Vezzani, Marga Behrens, Tamas Bartfai, Tallie Z. Baram

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)152-155
Number of pages4
JournalAnnals of Neurology
Issue number1
Publication statusPublished - Jan 2005

ASJC Scopus subject areas

  • Neuroscience(all)


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