Tumor Necrosis Factor-α Suppresses Sustained Potassium Currents in Rat Small Diameter Sensory Neurons
| Autor: | Bao-Gang Liu, Maxim Dobretsov, Jun-Ming Zhang, Joseph R. Stimers |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
business.industry
Potassium Neuroscience (miscellaneous) chemistry.chemical_element Cell biology Anesthesiology and Pain Medicine medicine.anatomical_structure Nociception Dorsal root ganglion chemistry Hyperalgesia medicine Tumor necrosis factor alpha Patch clamp medicine.symptom Prostaglandin E2 business Neuroscience Intracellular medicine.drug |
| Zdroj: | The Open Pain Journal. 1:1-7 |
| ISSN: | 1876-3863 |
| DOI: | 10.2174/1876386300902010001 |
| Popis: | Tumor necrosis factor- (TNF- ), 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- was examined in acutely dissociated small dorsal root ganglion neurons. We found that acute application of TNF- 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- 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- on potassium currents. These results suggest that TNF- 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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