| 李春梅,张大明,申东方,张淑岩,张 丽.乙酰胆碱参与大鼠尾核痛觉调制的机理研究[J].,2017,17(33):6427-6431 |
| 乙酰胆碱参与大鼠尾核痛觉调制的机理研究 |
| A Study on the Mechanism of Acetylcholine Involved in the Nociceptive Modulation in the Caudate Nucleus of Rats |
| 投稿时间：2017-08-09 修订日期：2017-08-31 |
| DOI：10.13241/j.cnki.pmb.2017.33.006 |
| 中文关键词: 尾核 乙酰胆碱 毛果芸香碱 阿托品 痛反应神经元 |
| 英文关键词: Caudate nucleus Acetylcholine Pilocarpine Atropine Pain-related neurons |
| 基金项目:黑龙江省教育厅科学技术研究项目（12521337） |
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| 中文摘要: |
| 摘要 目的：观察乙酰胆碱(ACh)对大鼠尾核痛反应神经元电活动的影响，探讨尾核在痛觉调制过程中与胆碱能系统的关系，为痛觉调节的中枢机制和镇痛治疗提供新的依据。方法：应用玻璃微电极细胞外记录的电生理学方法记录大鼠尾核内神经元放电，观察尾核内分别注入Ach、毛果芸香碱、阿托品、生理盐水等药物后痛反应神经元的放电表现，即痛兴奋神经元(PENs)的频率净增值(NIV)、潜伏期和痛抑制神经元(PINs)的NIV、抑制时程(ID)的改变。结果：大鼠尾核内注射ACh可以减少刺激坐骨神经诱发的尾核内痛相关神经元PENs的NIV，延长潜伏期，增加PINs的NIV，减少ID。尾核内注射毛果芸香碱后，产生和ACh类似的作用，而注射M受体阻断剂阿托品后则表现相反的效应。结论：外源性ACh能够调节大鼠尾核痛反应神经元的电活动，具有减弱痛觉在大鼠尾核中的传递作用，表现出镇痛效应，且可能主要与毒蕈碱受体途径有关。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effects of cholinergic agonists acetylcholine (ACh) on the pain-induced response of pain-related neurons in the caudate nucleus (Cd) of wistar rats, and find the mechanisms to reduce pain. Methods: Trains of electrical im- pulses applied to the sciatic nerve of rat were used as the noxious stimulus. The electrical activities of pain-excited neurons (PENs) or pain-inhibited neurons (PINs) in the Cd were recorded by a glass microelectrode. We recorded the net increased value (NIV) and latency of PENs, the NIV and inhibitory duration (ID) of PINs, after intra-Cd administration of ACh, pilocarpine, atropine and normal saline re- spectively. Results: The average NIV of PENs decreased and the average latency prolonged, the average NIV of PINs increased and the average ID shortened after the intra-Cd administration of ACh or pilocarpine. The average NIV of PENs increased and the average latency shortened, the average NIV of PINs decreased and the average ID prolonged after administration of atropine. Conclusion: ACh may play an analgesic role by affecting the electric activities of PENs and PINs, and the muscarinic pathway may be involved in the modulation of pain perception in the Cd. |
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