Intrathecal clonidine alleviates allodynia in neuropathic rats: interaction with spinal muscarinic and nicotinic receptors.
Intrathecal clonidine alleviates allodynia in neuropathic rats: interaction with spinal muscarinic and nicotinic receptors.
复制标题
鞘内可乐定减轻神经病大鼠的异常性疼痛：与脊髓毒蕈碱和烟碱受体的相互作用。
DOI：
10.1097/00000542-199902000-00027
复制
发表时间：
1999
期刊：
影响因子：
8.8
通讯作者：
Eisenach,JC
中科院分区：
文献类型：
--
作者：
Pan,HL;Chen,SR;Eisenach,JC
鞘内注射可乐定可增加脊髓乙酰胆碱的释放，这可能与其对神经病理性疼痛的镇痛作用有关。目前的研究确定脊髓毒蕈碱和烟碱受体的作用，在脊髓神经ligatedrates. MethodsAllydynia鞘内给药可乐定的抗异常性疼痛的影响，在大鼠左L5-L 6脊神经结扎。通过将von Frey细丝应用于左后爪来测定机械性异常性疼痛。鞘内注射生理盐水、两种毒蕈碱受体拮抗剂（阿托品和东莨菪碱）和两种烟碱受体拮抗剂（美加明和六甲铵）对鞘内注射20 μ g可乐定产生的抗异常性疼痛作用的影响在6组动物中进行了评估。每组由6至8 rats.ResultsIntrathecal注射生理盐水或毒蕈碱或烟碱受体拮抗剂没有改变的退缩阈值。鞘内注射可乐定产生的抗异常性疼痛作用以剂量依赖性方式通过鞘内注射毒蕈碱和烟碱拮抗剂治疗而减弱。虽然烟碱受体拮抗剂只有部分衰减可乐定的效果，脊髓毒蕈碱受体的封锁几乎取消了antiallodynic效应的可乐nidine.ConclusionsThese结果表明，神经病理性疼痛的镇痛作用鞘内给药可乐定是由脊髓毒蕈碱和烟碱受体介导的。因此，这项研究提供了功能证据，脊髓释放的乙酰胆碱发挥了作用，鞘内注射可乐定在神经病理性疼痛的抗异常性疼痛的效果。
BackgroundIntrathecally administered clonidine increases release of spinal acetylcholine, which may be related to its analgesic action in neuropathic pain. The current study determined the role of spinal muscarinic and nicotinic receptors in the antiallodynic effect of intrathecally administered clonidine in spinal nerve-ligated rats.MethodsAllodynia was produced in rats by ligation of the left L5-L6 spinal nerves. Mechanical allodynia was determined by application of von Frey filaments to the left hindpaw. The effect of intrathecal injection of saline, two muscarinic receptor antagonists (atropine and scopolamine), and two nicotinic receptor antagonists (mecamylamine and hexamethonium) on the antiallodynic action produced by intrathecal administration of 20 microg clonidine was assessed in six groups of animals. Each group consisted of six to eight rats.ResultsIntrathecal injection of saline or muscarinic or nicotinic receptor antagonists did not alter the withdrawal thresholds. The antiallodynic effect produced by intrathecally administered clonidine was attenuated in a dose-dependent manner by intrathecal treatment with muscarinic and nicotinic antagonists. Although nicotinic receptor antagonists only partially attenuated the effect of clonidine, blockade of spinal muscarinic receptors almost abolished the antiallodynic effect of clonidine.ConclusionsThese results demonstrate that the analgesic effect of intrathecally administered clonidine on neuropathic pain is mediated by spinal muscarinic and nicotinic receptors. Therefore, this study provides functional evidence that spinally released acetylcholine plays a role in the antiallodynic effect of intrathecally administered clonidine in neuropathic pain.