摘要
为观察尼氟灭酸（NFA）对坐骨神经慢性压迫损伤（CCI）所导致的神经病理性痛大鼠的背根神经节（dorsal root ganglion，DRG）神经元上GABAA 受体激活电流的影响，探讨尼氟灭酸在神经病理性疼痛时在脊髓水平的作用及可能机制。采用如下方法：（1）制作CCI模型。（2）运用热板实验检测CCI组、假手术组术侧下肢热缩足反射潜伏期的变化。（3）运用全细胞膜片钳技术记录CCI模型组术侧、假手术组术侧、正常组DRG神经元上GABAA受体激活电流的幅度。（4）记录尼氟灭酸对正常组和CCI组术侧DRG神经元上GABAA受体激活电流的调节作用。结果显示，（1）CCI组术侧下肢热缩足反射潜伏期明显缩短。（2）GABA（1-1000μmol/L ）可以使DRG 神经元产生浓度依赖的内向电流（P〈0.05,n=10）。（3）CCI组1-100μmol/L GABA激活电流幅值显著小于假手术组和正常对照组（P〈0.01，n=6）。假手术组和正常对照组GABA电流差异无统计学意义。（4）NFA（1-100μmol/L）对正常组、CCI组的DRG神经元上GABA激活的电流均有抑制作用，该抑制作用具有浓度依赖性，且正常组的抑制作用更明显（P〈0.01,n=5）。由此可知，NFA对CCI模型大鼠DRG神经元GABA激活电流的抑制作用相比较正常组有所减弱,这可能是由于CCI模型的DRG神经元上钙激活氯通道的数量增加。
To investigate the effects of niflumic acid （NFA） on GABA-activated currents in isolated dorsal root ganglion neurons in rats with neuropathic pain and explore the analgesia mechanism of NFA. （1） CCI mice model and the pseudo-operation model was established and the change of thermal withdrawal latency on operated side was detected by Hot-plate test. （2） Whole-cell patch-clamp technique was employed to record the changes of GABA-activated currents in the CCI model group, the pseudo-operation group and the control group.Results showed that：（1）The thermal withdrawal latency on operated side of the CCI model group was significantly shortened. （2）The GABA （1-1000 μmol/L） made the DRG neurons to produce concentration dependent inward currents （P〈0.05,n=6）. （3）The GABA-activated currents of injured side in CCI group were significantly decreased compared with the pseudo-operation and control groups （GABA concentration,1-100 μmol/L）（P〈0.01）.（4） The currents of control groups were decreased significantly compared with the CCI group by the same concentration of NFA （P〈0.05,n=5）.The attenuation of the effect of inhibition on GABA-activated currents by NFA is due to the increased numbers of the CaCCs on DRG neurons in CCI group.
出处
《石河子大学学报（自然科学版）》
CAS
2014年第2期193-197,共5页
Journal of Shihezi University(Natural Science)
基金
新疆兵团青年科技创新基金专项(2010JC33)
