基础医学与临床 ›› 2007, Vol. 27 ›› Issue (10): 1135-1139.

• 研究论文 • 上一篇    下一篇

N和M1受体介导乙酰胆碱对大鼠尾核痛兴奋神经元放电的抑制作用

王腾(黑龙江) 李玉荣 姚坤 刘松涛 曲丽辉 田华 金宏波   

  1. 哈尔滨医科大学生理学教研室 哈尔滨医科大学生理教研室 哈尔滨医科大学生理学教研室 哈尔滨医科大学生理学教研室 哈尔滨医科大学生理教研室 哈尔滨医科大学生理学教研室 哈尔滨医科大学生理学教研室
  • 收稿日期:2006-11-30 修回日期:1900-01-01 出版日期:2007-10-25 发布日期:2007-10-25
  • 通讯作者: 王腾(黑龙江)

N and M1 Receptors Mediated ACh-induced Inhibition of the Electric Discharge in Pain-excited Neurons of Caudate Nucleus of Rats

  

  • Received:2006-11-30 Revised:1900-01-01 Online:2007-10-25 Published:2007-10-25

摘要: 目的 研究不同胆碱能受体及其亚型在乙酰胆碱(ACh)对大鼠尾核痛兴奋神经元(PEN)放电影响中的作用。方法 以电脉冲刺激左侧坐骨神经作为伤害性刺激,用玻璃微电极细胞外记录神经元的放电变化,观察脑室注射ACh和M1、M3、M4以及N受体阻滞剂对尾核PEN电活动的影响。结果 (1)脑室注射ACh(20μg/10μl)可抑制大鼠尾核 PEN的电活动,使 PEN痛诱发放电频率减少,潜伏期延长;(2)ACh对PEN放电的抑制作用可被N受体阻滞剂筒箭毒碱(Tubocurare,0.8μg/10μl)和M1受体阻滞剂哌仑西平(Pirenzepine,10μg/10μl)所拮抗。(3)M3受体阻滞剂4-DAMP(10μg/10μl)和M4受体阻滞剂托品酰胺(Tropicamide, 10μg/10μl)不能拮抗ACh对PEN的抑制作用。结论 ACh参与尾核镇痛作用可能主要是通过N受体和M1受体介导。

Abstract: Objective To study the role of cholinergic receptors and their subtypes involved in the effects of acetylcholine (ACh) on the electric discharge of pain-excited neurons (PEN) in caudate nucleus of rat brain. Methods Trains of the electric impulses were applied to the left sciatic nerve as noxious stimulus ,the electric activities of PEN in caudate nucleus were recorded by extracelluar recording method with glass microelectrode after intracerebroventricular (i. c. v.) injection of ACh and muscarinic1 (M1) ,muscarinic3 (M3), muscarinic4 (M4) receptor antagonists and nAch-receptor antagonist. Results (1) I.c.v injection of ACh (20μg/10μl) showed the inhibitory effect of discharge of the PEN, resulted in the net-increased value (NIV) of frequency of induced discharge of the PEN decreased and the latency of the PEN lengthened. (2) This inhibition could be blocked by nAch-receptor antagonist (tubocurare ,0.8μg/10μl) and M1 receptor antagonist (pirenzepine,10μg/10μl). (3) This inhibition could not be blocked by M3 receptor antagonist (4-DAMP,10μg/10μl) and M4 receptor antagonist(tropicamide, 10μg/10μl). Conclusions The results suggested that it was maybe mediated mainly by nAch-receptor and M1 receptor that ACh produced the analgesic effects in caudate nucleus of rat brain.