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J Neurophysiol (November 30, 2005). doi:10.1152/jn.00509.2005
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Submitted on May 16, 2005
Accepted on November 19, 2005

CHRONIC IL-1{beta} SIGNALING POTENTIATES VOLTAGE DEPENDENT SODIUM CURRENTS IN TRIGEMINAL NOCICEPTIVE NEURONS

Lieju Liu1, T M Yang2, Wolfgang Liedtke3, and S A Simon4*

1 Department of Anesthesiology, Duke University, Durham, NC, USA
2 Department of Neurobiology, Duke University, Durham, NC, USA
3 Department of Neurobiology, Duke University, Durham, NC, USA; Department of Neurology, Duke University, Durham, NC, USA; Center for Translational Neuroscience, Duke University, Durham, NC, USA
4 Department of Anesthesiology, Duke University, Durham, NC, USA; Department of Neurobiology, Duke University, Durham, NC, USA; Center for Neuroengineering, Duke University, Durham, NC, USA

* To whom correspondence should be addressed. E-mail: sas{at}neuro.duke.edu.

The proinflammatory cytokine interleukin-1{beta} mediates inflammation and hyperalgesia. However, the underlying mechanisms remain elusive. To better understand such molecular and cellular mechanisms, we investigated how IL-1{beta} modulates the 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 20ng/ml IL-1{beta}. A brief exposure led to a 28% specific (receptor mediated) reduction of INa in these neurons, which were found to be 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 PKC 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-1{beta} signaling in nociceptive sensory neurons may be a critical component of inflammatory-associated hyperalgesia.




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