Plasticity in action of intrathecal clonidine to mechanical but not thermal nociception after peripheral nerve injury
Plasticity in action of intrathecal clonidine to mechanical but not thermal nociception after peripheral nerve injury
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DOI：
10.1097/00000542-200307000-00030
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发表时间：
2003-07-01
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：
Paqueron, X;Conklin, D;Eisenach, JC
背景：鞘内注射可乐定可减轻神经病理性疼痛动物模型的触觉异常性疼痛，这种作用可被阿托品阻断。然而，强直性脊髓胆碱能活性的作用及其与α 2-肾上腺素能系统在正常和神经病理条件下的相互作用，以及不同的感觉方法尚未得到系统的研究。作者研究了胆碱能受体参与正常和神经病动物的热和机械敏感性及其与鞘内可乐定的相互作用。正常大鼠和接受L5/L 6脊神经结扎的大鼠在鞘内施用生理盐水、毒蕈碱受体拮抗剂阿托品结果：阿托品、胆碱能神经元毒素和生理盐水均不改变基础缩痛阈值。在神经损伤的大鼠中，生理盐水和阿托品均不改变可乐定对热刺激的抗伤害作用，但阿托品可降低可乐定对von Frey细丝退缩阈值的作用（34 +/- 5.6 vs. 14 +/- 5.8 g [平均值+/- SEM]，生理盐水vs.阿托品; P < 0.05）和缩足阈的变化（174 ± 18 g vs. 137 ± 16 g，生理盐水vs.阿托品; P < 0.05）。这些数据表明，神经损伤后，机械，而不是热的镇痛依赖于毒蕈碱的相互作用，因为只有机械镇痛被拮抗阿托品鞘内可乐定。这些结果不支持神经损伤大鼠通过强直性释放乙酰胆碱来调节伤害性传递。
Background: Intrathecal clonidine reduces tactile allodynia in animal models of neuropathic pain, and this effect is blocked by atropine. However, the role of tonic spinal cholinergic activity and its interaction with alpha2-adrenergic systems in normal and neuropathic conditions and to different sensory methods has not been systematically examined. The authors examined cholinergic receptor involvement in thermal and mechanical sensitivity in normal and neuropathic animals and its interaction with intrathecal clonidine.Methods: Normal rats and rats that received L5/L6 spinal nerve ligation were tested with acute radiant heat, paw pressure, and punctate mechanical stimulation before and after the intrathecal administration of saline, the muscarinic receptor antagonist, atropine, or a toxin to destroy cholinergic neurons, and then after intrathecal clonidine.Results: Atropine, the cholinergic neuronal toxin, and saline did not alter baseline withdrawal thresholds. in nerve-injured rats, neither saline nor atropine altered antinociception from clonidine to a thermal stimulus, but atropine reduced the effect of clonidine to von Frey filament withdrawal threshold (34 +/- 5.6 vs. 14 +/- 5.8 g [mean +/- SEM], saline vs. atropine; P < 0.05) and to withdrawal threshold to paw pressure after clonidine (174 ± 18 g vs. 137 ± 16 g, saline vs. atropine; P < 0.05).Conclusions: These data suggest that after nerve injury, mechanical but not thermal antinociception from intrathecal clonidine relies on a muscarinic interaction, because only mechanical antinociception was antagonized by atropine. These results do not favor a regulation of nociceptive transmission by a tonic release of acetylcholine in nerve-injured rats.