神经药理学报

神经药理学报 ›› 2016, Vol. 6 ›› Issue (2): 1-6.DOI: 10.3969/j.issn.2095-1396.2016.02.001

• 研究论文 •    下一篇

大鼠背根神经节中卫星胶质细胞容量激活氯电流的分子基础及机制

焦晓翠，张海林   

  1. 河北医科大学药理教研室，石家庄，050000，中国
  • 出版日期:2016-04-26 发布日期:2016-05-10
  • 通讯作者: 张海林，男，教授，博士，博士生导师；研究方向：分子药理学；E-mail：zhanghl@hebmu.edu.cn
  • 作者简介:焦晓翠，女，硕士；研究方向：分子药理学；E-mail：jiaoxiaocuivip@163.com
  • 基金资助:

    国家自然科学基金资助项目（No.31270882），国家重点基础研究发展计划（973 计划）（No.2013CB531302）

Molecular Basis and Mechanism of Swelling-Activated Chloride Current in Satellite Glia Cells of Rat Dorsal Root Ganglion

JIAO Xiao-cui, ZHANG Hai-lin   

  1. Department of Pharmacology，Hebei Medical University，Shijiazhuang，050000，China
  • Online:2016-04-26 Published:2016-05-10
  • Contact: 张海林，男，教授，博士，博士生导师；研究方向：分子药理学；E-mail：zhanghl@hebmu.edu.cn
  • About author:焦晓翠，女，硕士；研究方向：分子药理学；E-mail：jiaoxiaocuivip@163.com
  • Supported by:

    国家自然科学基金资助项目（No.31270882），国家重点基础研究发展计划（973 计划）（No.2013CB531302）

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摘要： 目的：探讨大鼠背根神经节中卫星胶质细胞容量激活氯电流的分子基础及激活机制。方法：采用全细胞膜片钳技术记录大鼠背根神经节中卫星胶质细胞上容量激活氯电流并观察在螯合细胞内钙离子、阻断细胞膜嘌呤受体、特异性敲低跨膜蛋白16A（trans membrane protein 16A，TMEM16A）时对该电流的影响。结果：在细胞内高渗条件下，在大鼠背根神经节的卫星胶质细胞上可以记录到可被氯离子通道阻断剂阻断的内向电流即容量激活氯电流。利用慢病毒载体所携载的siRNA 特异性敲低TMEM16A 可显著抑制该电流。螯合细胞内钙离子浓度可抑制该电流的发生；阻断ATP 受体对该电流的发生无影响。结论：大鼠背根神经节的卫星胶质细胞上存在容量激活的氯电流，其分子基础为TMEM16A 介导的钙激活氯通道，激活机制可能与细胞内钙离子的释放有关。

关键词: 卫星胶质细胞, 容量激活氯电流, 钙离子, 跨膜蛋白16A

Abstract: Objective：To study the molecular basis and the mechanism of volumeactivated chloride currents （VACC） in the satellite glia cells （SGCs） of rat dorsal root ganglion （DRG）. Methods：The VACC was recorded by whole-cell patch clamp technique. Pharmacological tools were used to evaluate the roles of calcium and purinergic receptors in the activation of VACC. siRNA was used to evaluate the role of TMEM16A in the molecular basis of VACC. Results：Hypertonic intracellular solution induced an inward current that was blocked by chloride channel blocker in the SGCs of rat DRG. This current，namely VACC，was reduced significantly when SGCs were transfected with siRNA against TMEM16A. The development of VACC was blocked when the intracellular Ca2+ was chelated with high concentrations of BAPTA or EGTA. VACC was not affected when P2 receptor was blocked. Conclusions：The above results suggest that the SGCs in the rat DRG express VACC. The VACC is activated by the increase of cell volume involving release of intracellular calcium. TMEM16A proteins appear to be a crucial component of the VACC in rat SGCs.

Key words: satellite glia cells, volume-activated chloride channel, Ca2+, trans membrane protein 16A（ TMEM16A）

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