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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 000μmol/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 neuronal nicotinic receptor (nAChR) in primary sensory neurons. Methods The whole cell patch clamp technique was used to observe the modulation effect of artificial cannabinoid (WIN55, 212-2) on nicotine activation current on cultured trigeminal ganglion neurons. Results Most of the examined cells (82.5%, 85/103) were sensitive to nicotine (10 to 1 000 μmol/L), resulting in a concentration-dependent inward current; compared with the effect of nicotine alone, WIN55,212- 2 (0.03~30μmol/L) and nicotine can significantly inhibit the peak of nicotine activation current; and this rapid inhibition was reversible, concentration-dependent and non-voltage-dependent; WIN55,212-2 make the nicotine activation current dose effect The curve is clearly down, but there is no significant change in the EC50 value. Conclusions WIN55,212-2 can act directly on nAChR and inhibit the nicotine current in a non-competitive manner to exert peripheral analgesia.