...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Tetrodotoxin-resistant Na+ currents and inflammatory hyperalgesia
【24h】

Tetrodotoxin-resistant Na+ currents and inflammatory hyperalgesia

机译：抗河豚毒素的Na +电流和炎性痛觉过敏

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Several mechanisms have been identified that may underlie inflammation-induced sensitization of high-threshold primary afferent neurons, including the modulation of voltage-and Ca(2+)-dependent ion channels and ion channels responsible for the production of generator potentials. One such mechanism that has recently received a lot of attention is the modulation of a tetrodotoxin(TTX)-resistant voltage-gated Na+ current. Evidence supporting a role for TTX-resistant Na+ currents in the sensitization of primary afferent neurons and inflammatory hyperalgesia is reviewed. Such evidence is derived from studies on the distribution of TTX- TTX-resistant Na+ currents among primary afferent neurons and other tissues of the body that suggest that these currents are expressed only in a subpopulation of primary afferent neurons that are likely to be involved in nociception . Data from studies on the biophysical properties of these currents suggest that they are ideally suited to mediate the repetitive discharge associated with prolonged membrane depolarizations . Data from studies on the effects of inflammatory mediators and antinociceptive agents on TTX-resistant Na~+ currents suggest that modulation of these currents is an underlying mechanism of primary afferent neuron sensitization. In addition, the second-messenger pathways underlying inflammatory mediator-induced modulation of these currents appear to underlie inflammatory mediator-induced hyperalgesia. Finally, recent antisense studies have also yielded data supporting a role for TTX-resistant Na(+) currents in inflammatory hypera
机译：已经确定了几种机制可能是炎症诱导的高阈值初级传入神经元致敏的基础，包括对电压和Ca（2+）依赖性离子通道和负责产生发生器电势的离子通道的调节。最近受到广泛关注的一种这样的机制是抗河豚毒素（TTX）的电压门控Na +电流的调节。综述了支持TTX抗性Na +电流在原发传入神经元和炎症性痛觉过敏致敏中作用的证据。此类证据来自对原发传入神经元和身体其他组织之间的TTX- TTX耐药性Na +电流分布的研究，这些研究表明这些电流仅在可能与伤害感受有关的原发传入神经元亚群中表达。有关这些电流的生物物理特性的研究数据表明，它们非常适合介导与长时间的膜去极化相关的重复放电。关于炎症介质和抗伤害感受药对耐TTX的Na〜+电流的影响的研究数据表明，这些电流的调节是初级传入神经元敏化的潜在机制。另外，炎症介质诱导的这些电流的调节的第二信使途径似乎是炎症介质诱导的痛觉过敏的基础。最后，最近的反义研究也得出了支持TTX耐药性Na（+）电流在炎性增生中起作用的数据。

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