IL‐1J potentiates heat‐activated currents in rat sensory neurons: involvement of IL‐1RI, tyrosine kinase, and protein kinase C

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Abstract
Interleukin 1β (IL‐1β) is a proinflammatory cytokine that maintains thermal hyperalgesia and facilitates the release of calcitonin gene‐related peptide from rat cutaneous nociceptors in vivo and in vitro. Brief applications of IL‐1β to nociceptive neurons yielded a potentiation of heat‐activated inward currents (Iheat) and a shift of activation threshold toward lower temperature without altering intracellular calcium levels. The IL‐1β‐induced heat sensitization was not dependent on G‐protein‐coupled receptors but was mediated by activation of protein kinases. The nonspecific protein kinase inhibitor staurosporine, the specific protein kinase C inhibitor bisindolylmaleimide BIM1, and the protein tyrosine kinase inhibitor genistein reduced the sensitizing effect of IL‐1β whereas negative controls were ineffective. RT‐PCR and in situ hybridization revealed IL‐1RI but not RII expression in neurons rather than surrounding satellite cells in rat dorsal root ganglia. IL‐1β acts on sensory neurons to increase their susceptibility for noxious heat via an IL‐1RI/PTK/ PKC‐dependent mechanism.—Obreja, O., Rathee, P. K., Lips, K. S., Distler, C., Kress, M. IL‐1J potentiates heat‐activated currents in rat sensory neurons: involvement of IL‐1RI, tyrosine kinase, and protein kinase C. FASEB J. 16, 1497–1503 (2002)
Funding Information
  • California Department of Fish and Game (SFB 353, A10)
  • Wilhelm Sander-Stiftung (1996.058.2)