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首页> 外文期刊>The journal of physiological sciences: JPS >Spinal cholinergic mechanism of the relieving effects of electroacupuncture on cold and warm allodynia in a rat model of neuropathic pain.
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Spinal cholinergic mechanism of the relieving effects of electroacupuncture on cold and warm allodynia in a rat model of neuropathic pain.

机译:在神经性疼痛大鼠模型中电针缓解冷热痛觉过敏的脊髓胆碱能机制。

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摘要

This study was performed to determine whether spinal cholinergic systems mediate the relieving effects of electroacupuncture (EA) on cold and warm allodynia in a rat model of neuropathic pain. For neuropathic surgery, the right superior caudal trunk was resected at the level between the S1 and S2 spinal nerves innervating the tail. Two weeks after the injury, the intrathecal (i.t.) catheter was implanted. Five days after the catheterization, the rats were injected with atropine (non-selective muscarinic antagonist, 30 microg), mecamylamine (non-selective nicotinic antagonist, 50 microg), pirenzepine (M(1) muscarinic antagonist, 10 microg), methoctramine (M(2) antagonist, 10 microg) or 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) (M(3) antagonist, 10 microg). Ten minutes after the injection, EA was applied to the ST36 acupoint for 30 min. The cold and warm allodynia were assessed by the tail immersion test [i.e., immersing the tail in cold (4 degrees C) or warm (40 degrees C) water and measuring the latency of an abrupt tail movement] before and after the treatments. The i.t. atropine, but not mecamylamine, blocked the relieving effects of EA on cold and warm allodynia. Furthermore, i.t. pirenzepine attenuated the antiallodynic effects of EA, whereas methoctramine and 4-DAMP did not. These results suggest that spinal muscarinic receptors, especially M(1) subtype, mediate the EA-induced antiallodynia in neuropathic rats.
机译:进行这项研究以确定在神经性疼痛的大鼠模型中,脊髓胆碱能系统是否介导了电针(EA)对冷和热异常性疼痛的缓解作用。对于神经外科手术,在支配尾巴的S1和S2脊神经之间的水平切除右上尾干。受伤两周后,植入鞘内(i.t.)导管。导管插入后五天,给大鼠注射阿托品(非选择性毒蕈碱拮抗剂,30微克),美卡敏(非选择性烟碱拮抗剂,50微克),哌仑西平(M(1)毒蕈碱拮抗剂,10微克),甲基辛卡明( M(2)拮抗剂10微克)或4-二苯基乙酰氧基-N-甲基哌啶甲硫醚(4-DAMP)(M(3)拮抗剂10微克)。注射后十分钟,将EA应用于ST36穴位30分钟。在治疗之前和之后,通过尾巴浸没试验[即将尾巴浸入冷的(4℃)或温热的(40℃)水中并测量突然的尾巴运动的潜伏期]评估冷和热的异常性疼痛。 i.t.阿托品,但不是美卡明胺,阻止了EA对冷热性痛觉过敏的缓解作用。此外,i.t。哌仑西平减弱了EA的抗痛觉过敏作用,而甲辛胺和4-DAMP则没有。这些结果表明,脊髓毒蕈碱受体,特别是M(1)亚型,介导EA诱导的神经性大鼠的抗异常性疼痛。

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