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加巴喷丁对神经病理性痛大鼠背根神经节神经元高电压激活钙电流的影响
引用本文:陈晓东,朱敏敏,安珊珊,王强,陆亮,孙芹,肖杭,徐建国,段满林.加巴喷丁对神经病理性痛大鼠背根神经节神经元高电压激活钙电流的影响[J].中华麻醉学杂志,2010,30(1).
作者姓名:陈晓东  朱敏敏  安珊珊  王强  陆亮  孙芹  肖杭  徐建国  段满林
作者单位:1. 徐州医学院江苏省麻醉学重点实验室,221002
2. 南京军区南京总医院麻醉科
3. 医科大学现代毒理学教育部重点实验室
摘    要:目的 评价加巴喷丁对神经病理性痛大鼠背根神经节神经元高电压激活钙电流的影响.方法 雄性SD大鼠,周龄4~6周,采用结扎L_5脊神经的方法建立神经病理性痛模型.于术后14 d时采用酶消化法急性分离损伤侧L_5背根神经节神经元,采用全细胞膜片钳技术记录神经元高电压激活钙电流,记录加巴喷丁0.1、1、10、100、300 μmol/L(G_(1~5)组)作用下的钙电流,计算电流抑制率;并绘制100 μmol/L加巴喷丁作用下钙电流-电压曲线、钙通道激活曲线和稳态失活曲线.结果 与给药前比较,G_(1~5)组给药后钙电流均降低(P<0.05).给予100 μmol/L加巴喷丁后钙电流-电压曲线左移.与给药前比较,给予100 μmol/L加巴喷丁后钙通道激活曲线的半数激活电压和稳态失活曲线的半数失活电压降低(P<0.05),激活曲线向超级化方向移动3.47 mV,稳态失活曲线向超极化方向移动9.32 mV.结论 加巴喷丁可抑制神经病理性痛大鼠背根神经节神经元高电压激活钙电流,可能与其抑制钙通道的失活特性有关.

关 键 词:环己酸类  钙通道  神经痛  神经节    神经元

Effects of gabapentin on high voltage active calcium currents in injured dorsal root ganglion neurons in a rat model of neuropathic pain
CHEN Xiao-dong,ZHU Min-min,AN Shan-shan,WANG Qiang,LU Liang,SUN Qin,XIAO Hang,XU Jian-guo,DUAN Man-lin.Effects of gabapentin on high voltage active calcium currents in injured dorsal root ganglion neurons in a rat model of neuropathic pain[J].Chinese Journal of Anesthesilolgy,2010,30(1).
Authors:CHEN Xiao-dong  ZHU Min-min  AN Shan-shan  WANG Qiang  LU Liang  SUN Qin  XIAO Hang  XU Jian-guo  DUAN Man-lin
Abstract:Objective To investigate the effect of gabapentin on high voltage active calcium currents in the injured dorsal root ganglion (DRG) neurons in a rat model of neuropathic pain.Methods Pathogen-free male SD rats aged 4-6 weeks were used in this study. The animals were anesthetized with intraperitoneal pentobarbital soclium 50 mg/kg. L_5 spinal nerve was ligated between DRG and sciatic nerve and cut distal to the ligature. The animals were decapitated on the 14th postoperative day. L_5 DRG was isolated and the neurons in the ganglion were enzymatically dissociated. The high voltage active calcium current was recorded using whole-cell patch-clamp technique.Results Gabapentin inhibited the peak calcium current in the injured DEG neurons. Peak calcium current was decreased by gabapentin 100 μmol/L and both activation and steady-state inactivation curve shifted to more hyperpolarized potentials. Conclusion Gabapentin can inhibit high voltage active in the injured DRG neurons in a rat model of neuropathic pain. The alteration in the inactivation of the electrophysiological properties may be involved in the mechanism.
Keywords:Cyclohexanecarboxylic acids  Calcium channels  Neuralgia  Ganglia  spinal  Neurons
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