RESEARCH ARTICLE
Tumor Necrosis Factor-α Suppresses Sustained Potassium Currents in Rat Small Diameter Sensory Neurons
Bao-Gang Liu2, , Maxim Dobretsov2, Joseph R. Stimers3, Jun-Ming Zhang*, 1, 2
Article Information
Identifiers and Pagination:
Year: 2008Volume: 1
First Page: 1
Last Page: 7
Publisher ID: TOPAINJ-1-1
DOI: 10.2174/1876386300902010001
Article History:
Received Date: 10/10/2008Revision Received Date: 23/10/2008
Acceptance Date: 27/10/2008
Electronic publication date: 18/11/2008
Collection year: 2008
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Tumor necrosis factor-α (TNF-α), a pro-inflammatory cytokine, produces pain and hyperalgesia by activating and/or sensitizing nociceptive sensory neurons. In the present study, using whole-cell patch clamp techniques, the regulation of potassium currents by TNF-α was examined in acutely dissociated small dorsal root ganglion neurons. We found that acute application of TNF-α inhibited, in a dose-dependent manner, the non-inactivating sustained potassium current without changing the rapidly inactivating transient current or the voltage-dependence of steady-state inactivation. The effects of TNF-α on potassium currents were similar to that of prostaglandin E2 as reported previously and also demonstrated in the current study. Furthermore, indomethacin, a potent inhibitor for both cyclo-oxygenase (COX)-1 and COX-2, completely blocked the effect of TNF-α on potassium currents. These results suggest that TNF-α may sensitize or activate sensory neurons by suppressing the sustained potassium current in nociceptive DRG neurons, possibly via stimulating the intracellular production i.e. the synthesis and/or release of endogenous prostaglandins.