Zhu He, Ma Ke-tao, Li Li, Zhang Zhong-shuang, Li Jing, Si Jun-qiang
The key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University Medical College, Shihezi 832002, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2011 Aug;27(3):376-9.
To investigate the changes of GABA-activated currents in isolated dorsal root ganglion neurons in rats with neuropathic pain.
The neuropathic pain model was established by chronic constriction injury (CCI) 7 days before electrophysiological-recording. The rat DRG neurons were enzymatically dissociated. Whole-cell patch clamp technique was used to record GABA-activated currents. The changes of currents of injured side and opposite side were expected to compare with control group.
(1) The currents of injured side of CCI group were notablely decreased compared with control group (GABA concentration, 0.1-1000 micromol/L). (2) By the contrast, opposite side currents of CCI group increased significantly compared with those in injured side and control group (GABA concentration, 0.01-1000 micromol/L).
The data indicates that the chronic constriction injury change both the function of GABAA receptors of injury side and opposite side. The decrease of pre-synaptic inhibition of GABA may be the possible reason of neuropathic pain.
研究神经病理性疼痛大鼠离体背根神经节神经元中γ-氨基丁酸(GABA)激活电流的变化。
在电生理记录前7天,通过慢性缩窄损伤(CCI)建立神经病理性疼痛模型。将大鼠背根神经节神经元进行酶解分离。采用全细胞膜片钳技术记录GABA激活电流。预期比较损伤侧和对侧电流的变化与对照组。
(1)与对照组相比,CCI组损伤侧电流显著降低(GABA浓度为0.1 - 1000微摩尔/升)。(2)相比之下,CCI组对侧电流与损伤侧及对照组相比显著增加(GABA浓度为0.01 - 1000微摩尔/升)。
数据表明慢性缩窄损伤改变了损伤侧和对侧GABAA受体的功能。GABA突触前抑制的降低可能是神经病理性疼痛的可能原因。