摘要
目的:观察大鼠坐骨神经慢性压迫性损伤(chronic constriction injury CCI)致神经病理性痛后,咪达唑仑对背根神经节(dorsal root ganglion,DRG)神经元上γ-氨基丁酸A受体(gamma-aminobutyricacid A receptor,GABA-AR)激活电流的调控作用。方法:运用全细胞膜片钳技术,记录假手术、CCI组、正常组GABA-AR激活电流的变化、以及咪达唑仑对坐骨神经慢性压迫性损伤后GABA-AR激活电流的影响。结果:CCI组GABA(0.1～1000μmol/L)激活的电流幅值显著小于假手术组和正常组。假手术组和正常组由GABA(0.1～1000μmol/L)激活的电流幅值差异无统计学意义。不同浓度咪达唑仑(0.03～100μmol/L)对CCI组GABA-AR激活电流均有增强作用,且随咪达唑仑浓度升高,对DRG神经元GABA-AR激活电流的增强率逐渐升高,3.00μmol/L咪达唑仑时达峰值(P<0.05或0.01)。结论:在CCI组中,DRG神经元GABA-AR功能的改变导致的突触前抑制作用的减弱可能是疼痛产生的关键因素之一。咪达唑仑对CCI组GABA-AR功能有增强作用,增强GABA-AR参与突触前抑制作用,可能是其在脊髓水平产生镇痛的机制之一。
Objective： To investigate the changes of gamma-aminobutyric acid A receptor（GABA-AR） activated currents by Midazolam in isolated dorsal root ganglion neurons in rats with neuropathic pain.Methods： The neuropathic pain model was established by chronic constriction injury（CCI） 7 days before electrophysiological recording.Whole-cell patch-clamp technique was used to record the changes of GABAAR activated currents in rats with neuropathic pain.Results： The currents of injured side of CCI group were significantly decreased compared with the pseudo-operation and NC groups（GABA concentration,0.1 ~ 1000μmol/L）.The difference of currents between the pseudo-operation and NC groups was not statistically significant.By Midazolam,the currents of CCI group increased significantly compared with the NC groups.Conclusion： The decrease of presynaptic inhibition of GABA may be the possible reason of neuropathic pain.The enhancement of currents by Midazolam of CCI group may increase GABA-AR mediated presynaptic inhibition at the spinal cord level.
出处
《中国疼痛医学杂志》
CAS
CSCD
北大核心
2013年第6期330-335,共6页
Chinese Journal of Pain Medicine
基金
兵团青年科技创新基金专项(2010JC33)
关键词
咪达唑仑
神经病理性痛
背根神经节
Γ-氨基丁酸A受体
全细胞膜片钳
Midazolam
Neuropathic pain
Dorsal root ganglion（DRG）
Gamma-aminobutyric acid Areceptor （GABA-AR）
Whole-cell patch-clamp
