Chronic IL-1beta signaling potentiates voltage-dependent sodium currents in trigeminal nociceptive neurons.

Journal Article (Journal Article)

The proinflammatory cytokine interleukin-1beta (IL-1beta) mediates inflammation and hyperalgesia, although the underlying mechanisms remain elusive. To better understand such molecular and cellular mechanisms, we investigated how IL-1beta modulates the total voltage-dependent sodium currents (INa) and its tetrodotoxin-resistant (TTX-R) component in capsaicin-sensitive trigeminal nociceptive neurons, both after a brief (5-min) and after a chronic exposure (24-h) of 20 ng/ml IL-1beta. A brief exposure led to a 28% specific (receptor-mediated) reduction of INa in these neurons, which were found to contain type I IL-1 receptors (IL-1RI+) on both their soma and nerve endings. In marked contrast, after a 24-h exposure, the total sodium current was specifically increased by 67%, without significantly affecting the TTX-R component. This potentiation of INa was suppressed in the presence of selective inhibitors of protein kinase C and G-protein-coupled signaling pathways, thereby suggesting that INa can be modulated through multiple pathways. In summary, the potentiation of INa through chronic IL-1beta signaling in nociceptive sensory neurons may be a critical component of inflammatory-associated hyperalgesia.

Full Text

Duke Authors

Cited Authors

  • Liu, L; Yang, TM; Liedtke, W; Simon, SA

Published Date

  • March 2006

Published In

Volume / Issue

  • 95 / 3

Start / End Page

  • 1478 - 1490

PubMed ID

  • 16319216

International Standard Serial Number (ISSN)

  • 0022-3077

Digital Object Identifier (DOI)

  • 10.1152/jn.00509.2005


  • eng

Conference Location

  • United States