Acta Neuropharmacologica››2015,Vol. 5››Issue (5): 49-56.

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Progress of Voltage Gated Sodium Channel Nav1.7 and its Specific Blockers in Nneuropathic pain

WANG Chuan,SHAN Bin,WANG Qiong,ZHANG Hai-lin

  1. 1. Department of Pharmacology, Hebei Medical University, Shijiazhuang, 050017, China
    2. Department of Pharmacy, the Forth Hospital of Hebei Medical University , Shijiazhuang, 050011, China
  • Online:2015-10-26Published:2016-03-03
  • Contact:张海林,男,博士,教授,博士生导师;研究方向:神经药理学;Tel: +86-0311-86265562, E-mail: zhanghl@hebmu.edu.cn
  • About author:王川,男,博士,教授,博士生导师;研究方向:分子药理学;Tel: +86-0311-86261031, E-mail: wangchuan@hebmu.edu.cn
  • Supported by:

    国家自然科学基金资助项目(No.31171097,No.31270882),国家重点基础研究发展计划(973计划)(2013CB531302), 河北省自然科学基金资助项目(No.C2014206419),教育部留学回国人员科研启动基金项目(2013-693),河北省高等学校科学技术研究项目重点项目(ZD2015007)

Abstract:Voltage gated sodium channels (Nav) play important roles in generation and conduction of pain. In pain conduction pathway, Nav1.7 is selectively expressed in small-diameter peripheral somatic sensory neurons and sympathetic ganglion neurons. Nav1.7 modulates neuronal excitability through amplifing subthreshold of depolarizations and setting up the thresholds of Nav1.8 and Nav1.9. This review will focus on the progress of neuropathic pain caused by mutations in Nav1.7. Nav1.7 can be used as an effective target for the treatment of pain. Highly selective Nav1.7 blockers will be of great clinical value in the treatment of pain.

Key words:neuropathic pain,voltage gated sodium channel,Nav1.7,sodium channel blocker,dorsal root ganglia,channel structure

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