• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Open Pain Journal >Tumor Necrosis Factor-α Suppresses Sustained Potassium Currents in Rat Small Diameter Sensory Neurons
【24h】

Tumor Necrosis Factor-α Suppresses Sustained Potassium Currents in Rat Small Diameter Sensory Neurons

机译：肿瘤坏死因子-α抑制大鼠小直径感觉神经元的持续钾电流。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

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.
机译：促炎细胞因子肿瘤坏死因子-α（TNF-α）通过激活和/或敏化伤害性感觉神经元而产生疼痛和痛觉过敏。在本研究中，使用全细胞膜片钳技术，在急性分离的小背根神经节神经元中检测了TNF-α对钾电流的调节。我们发现，TNF-α的急性应用以剂量依赖的方式抑制了非灭活的持续钾电流，而没有改变快速灭活的瞬态电流或稳态灭活的电压依赖性。 TNF-α对钾电流的影响与以前报道的前列腺素E2相似，本研究也证实了这一点。此外，吲哚美辛，一种强力的环氧化酶（COX）-1和COX-2抑制剂，完全阻断了TNF-α对钾电流的作用。这些结果表明，TNF-α可通过抑制伤害性DRG神经元中的持续钾电流，可能通过刺激细胞内产生即内源性前列腺素的合成和/或释放，来敏化或激活感觉神经元。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号