中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2012, Vol. 7 ›› Issue (32): 2492-2499.

• 原著:周围神经损伤修复保护与再生 • 上一篇    下一篇

坐骨神经损伤大鼠背根神经节中γ-氨基丁酸A型受体α2亚基的表达

  

  • 收稿日期:2012-08-08 修回日期:2012-10-23 出版日期:2012-11-15 发布日期:2012-11-15

Expression of gamma-aminobutyric acid type A receptor α2 subunit in the dorsal root ganglion of rats with sciatic nerve injury

Yu Lian 1, 2, Yang Wang 1, 2, 3, Ketao Ma 1, 2, Lei Zhao 1, 2, Zhongshuang Zhang 1, 2, Yuanyuan Shang 1, 2,Junqiang Si 1, 2, 3, Li Li 1, 2   

  1. 1 Department of Physiology, Shihezi University School of Medicine, Shihezi 832002, Xinjiang Uygur Autonomous Region,China
    2 Key Laboratory of Xinjiang Endemic and Ethnic Disease, Shihezi University School of Medicine, Shihezi 832002,Xinjiang Uygur Autonomous Region, China
    3 Fundamental Medical School of Wuhan University, Wuhan 430071, Hubei Province, China
  • Received:2012-08-08 Revised:2012-10-23 Online:2012-11-15 Published:2012-11-15
  • Contact: Li Li,M.D., Associate professor,Department of Physiology,Shihezi University School of Medicine, Shihezi 832002,Xinjiang Uygur Autonomous Region, China; Key Laboratory of Xinjiang Endemic and Ethnic Disease,Shihezi University School of Medicine, Shihezi 832002,Xinjiang Uygur Autonomous Region, China; Junqiang Si,M.D., Professor, Department of Physiology, Shihezi University School of Medicine, Shihezi 832002,Xinjiang Uygur Autonomous Region, China; Key Laboratory of Xinjiang Endemic and Ethnic Disease,Shihezi University School of Medicine, Shihezi 832002,Xinjiang Uygur Autonomous Region, China; Fundamental Medical School of Wuhan University, Wuhan 430071,Hubei Province, China Lily7588@163.com;sijunqiang@shzu.edu.cn
  • About author:Yu Lian★, Master,Department of Physiology,Shihezi University School of Medicine, Shihezi 832002,Xinjiang Uygur Autonomous Region, China; Key Laboratory of Xinjiang Endemic and Ethnic Disease,Shihezi University School of Medicine, Shihezi 832002,Xinjiang Uygur Autonomous Region, China

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Abstract:

The γ-aminobutyric acid neurotransmitter in the spinal cord dorsal horn plays an important role in pain modulation through primary afferent-mediated presynaptic inhibition. The weakening of γ-aminobutyric acid-mediated presynaptic inhibition may be an important cause of neuropathic pain.γ-aminobutyric acid-mediated presynaptic inhibition is related to the current strength of γ-aminobutyric acid A receptor activation. In view of this, the whole-cell patch-clamp technique was used here to record the change in muscimol activated current of dorsal root ganglion neurons in a chronic constriction injury model. Results found that damage in rat dorsal root ganglion neurons following application of muscimol caused concentration-dependent activation of current, and compared with the sham group, its current strength and γ-aminobutyric acid A receptor protein expression decreased. Immunofluorescence revealed that γ-aminobutyric acid type A receptor α2 subunit protein expression decreased and was most obvious at 12 and 15 days after modeling. Our experimental findings confirmed that the γ-aminobutyric acid type A receptor α2 subunit in the chronic constriction injury model rat dorsal root ganglion was downregulated, which may be one of the reasons for the reduction of injury in dorsal root ganglion neurons following muscimol-activated currents.

Key words: γ-aminobutyric acid, γ-aminobutyric acid type A receptor α2 subunit, neuropathic pain, dorsal root ganglion, whole-cell patch clamp, immunofluorescence, primary afferent depolarization, paw withdrawal latency, muscimol