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

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Abstract
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.
Funding Information
  • NIH (National Institute of Mental Health)
  • National Institute of Neurological Disorders and Stroke (NS28912, NS35439, R01 NS043501)
  • Ellison Foundation
  • Epilepsy Foundation of America postdoctoral research fellowship (EP-36421)