大麻素对大鼠三叉神经节神经元烟碱激活电流的抑制作用  

Cannabinoid inhibits nicotine-activated currents in rat trigeminal ganglion neurons

作　　者：陆永利[1] 刘长金[1] 李爱[1] 胡新武[1] 

机构地区：[1]华中科技大学同济医学院生理系,武汉460030

出　　处：《卒中与神经疾病》2005年第5期272-274,277,共4页Stroke and Nervous Diseases

摘　　要：目的在初级感觉神经元上探讨大麻素对神经元烟碱受体(nAChR)的影响.方法应用全细胞膜片钳技术在培养的三叉神经节神经元上观察人工合成大麻素(WIN55,212-2)对烟碱激活电流的调制作用.结果大部分受检细胞(82.5%,85/103)对外加烟碱(10～1 000 μmol/L)敏感,产生一浓度依赖性内向电流;与烟碱单独作用相比,同时给予WIN55,212-2(0.03～30μmol/L)和烟碱能明显抑制烟碱激活电流峰值;且此快速抑制作用呈可逆性、浓度依赖性和非电压依赖性;WIN55,212-2使烟碱激活电流量效曲线明显下移,但EC50值无明显改变.结论WIN55,212-2可直接作用于nAChR,且以非竞争性方式抑制烟碱电流发挥外周镇痛作用.Objective To investigate the effect of cannabinoid on nAChR in primary sensory neurons. Methods By means of whole-cell patch clamp technique, the modulatory effect of synthetic cannabinoid WIN55,212-2 on nicotine-activated currents （Inic） was investigated in cultured rat trigeminal ganglion （TG） neurons. Results The majority of the neurons examined （82. 5%, 85/103） were sensitive to nicotine （10-1000μmol/L）. Nicotine activated a concentration-dependent inward current. Coappliation of WIN55, 212-2 （0. 03-30 μmol/L） and nicotine （100 μmol/L） inhibited Inic obviously. The rapid effect induced by WIN55, 212-2 was reversible, concentration, dependent and voltage-independent. WIN55, 212-2 shifted the nicotine dose-response curve downward and decreased the maximum without changing EC50 values （61.09 vs. 65.02 μmol/L）. Conclusions WIN55,212-2 inhibited nicotine-activated currents directly via nACh receptor and the inhibitory is non-competitive. It indicated that in periphery nervous system cannabinoid may play a role in antiociception by inhibiting nicotine-activated current.

关 键 词：大麻素 神经元烟碱受体 全细胞膜片钳 

分 类 号：R338[医药卫生—人体生理学] R745[医药卫生—基础医学]