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Brain Advance Access published online on April 7, 2005
Brain, doi:10.1093/brain/awh490
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received July 6, 2004
Revised December 23, 2004
Accepted February 28, 2005

Article

Fast modulation of heat-activated ionic current by proinflammatory interleukin 6 in rat sensory neurons

O. Obreja 1, W. Biasio 2, M. Andratsch 2, K. S. Lips 3, P. K. Rathee 1, A. Ludwig 4, S. Rose-John 4, and M. Kress 5*

1 Institut für Physiologie und Experimentelle Pathophysiologie, Friedrich-Alexander Universität, Erlangen-Nürnberg, Germany
2 Department für Physiologie und Medizinische Physik, Division Physiologie, Medizinische Universität, Innsbruck, Austria
3 Institut für Anatomie und Zellbiologie, Justus-Liebig Universität, Giessen, Germany
4 Institut für Biochemie, Christian-Albrecht Universität, Kiel, Germany
5 Institut für Physiologie und Experimentelle Pathophysiologie, Friedrich-Alexander Universität, Erlangen-Nürnberg, Germany; Department für Physiologie und Medizinische Physik, Division Physiologie, Medizinische Universität, Innsbruck, Austria

* To whom correspondence should be addressed.
M. Kress, E-mail: michaela.kress{at}uibk.ac.at


  Abstract

The pro-inflammatory cytokine interleukin-6 (IL-6) together with its soluble receptor (sIL-6R) induces and maintains thermal hyperalgesia. It facilitates the heat-induced release of calcitonin gene-related peptide from rat cutaneous nociceptors in vivo and in vitro. Here we report that exposure of nociceptive neurons to the IL-6-sIL-6R complex or the gp130-stimulating designer IL-6-sIL-6R fusion protein Hyper-IL-6 (HIL-6) resulted in a potentiation of heat-activated inward currents (Iheat) and a shift of activation thresholds towards lower temperatures without affecting intracellular calcium levels. The Janus tyrosine kinase inhibitor AG490, the selective protein kinase C (PKC) inhibitor, bisindolylmaleimide 1 (BIM1), as well as rottlerin, a selective blocker of the PKC{delta} isoform, but not the cyclooxygenase inhibitor indomethacin, effectively reduced the effect. Reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization revealed expression of mRNA for the signal-transducing {beta} subunit of the receptor gp130 in neuronal somata, rather than satellite cells in rat dorsal root ganglia. Together, the results suggest that IL-6-sIL-6R acts directly on sensory neurons. It increases their susceptibility to noxious heat via the gp130/Jak/PKC{delta} signalling pathway.

Keywords: thermal hyperalgesia; neuropathic pain; TRPV-1; vanilloid receptor; protein kinase.
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