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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Involvement of spinal muscarinic and serotonergic receptors in the anti-allodynic effect of electroacupuncture in rats with oxaliplatin-induced neuropathic pain
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Involvement of spinal muscarinic and serotonergic receptors in the anti-allodynic effect of electroacupuncture in rats with oxaliplatin-induced neuropathic pain

机译：脊髓毒蕈碱和血清素能受体参与电针对奥沙利铂诱导的神经性疼痛大鼠的抗痛觉异常作用

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This study was performed to investigate whether the spinal cholinergic and serotonergic analgesic systems mediate the relieving effect of electroacupuncture (EA) on oxaliplatin-induced neuropathic cold allodynia in rats. The cold allodynia induced by an oxaliplatin injection (6 mg/kg, i.p.) was evaluated by immersing the rat's tail into cold water (4℃) and measuring the withdrawal latency. EA stimulation (2 Hz, 0.3-ms pulse duration, 0.2~0.3 mA) at the acupoint ST36, GV3, or LI11 all showed a significant anti-allodynic effect, which was stronger at ST36. The analgesic effect of EA at ST36 was blocked by intraperitoneal injection of muscarinic acetylcholine receptor antagonist (atropine, 1 mg/kg), but not by nicotinic (mecamylamine, 2 mg/kg) receptor antagonist. Furthermore, intrathecal administration of M2 (methoctramine, 10 μg) and M3 (4-DAMP, 10 μg) receptor antagonist, but not M1 (pirenzepine, 10 μg) receptor antagonist, blocked the effect. Also, spinal administration of 5-HT3 (MDL-72222, 12 μg) receptor antagonist, but not 5-HT1A (NAN-190, 15 μg) or 5-HT2A (ketanserin, 30 μg) receptor antagonist, prevented the anti-allodynic effect of EA. These results suggest that EA may have a signifi cant analgesic action against oxaliplatin-induced neuropathic pain, which is mediated by spinal cholinergic (M2, M3) and serotonergic (5-HT3) receptors.
机译：进行这项研究以调查脊髓胆碱能和5-羟色胺能镇痛系统是否介导电针（EA）对奥沙利铂诱导的神经性冷异常性疼痛的缓解作用。通过将大鼠的尾巴浸入冷水（4℃）中并测量戒断潜伏期来评估由奥沙利铂注射液（6 mg / kg，腹膜内注射）诱发的冷异常性疼痛。 ST36，GV3或LI11穴位的EA刺激（2 Hz，0.3 ms脉冲持续时间，0.2〜0.3 mA）都显示出显着的抗痛觉异常作用，在ST36处更强。腹腔注射毒蕈碱型乙酰胆碱受体拮抗剂（阿托品，1 mg / kg）可阻断EA对ST36的镇痛作用，但烟碱类（甲基卡明胺，2 mg / kg）受体拮抗剂则不会阻断EA的镇痛作用。此外，鞘内注射M 2 （甲基辛巴胺，10μg）和M 3 （4-DAMP，10μg）受体拮抗剂，但不给予M 1 （哌仑西平，10μg）受体拮抗剂，阻断了该作用。此外，脊柱给药5-HT 3 （MDL-72222，12μg）受体拮抗剂，但不给药5-HT 1A （NAN-190，15μg）或5 -HT 2A （ketanserin，30μg）受体拮抗剂可预防EA的抗痛觉过敏作用。这些结果表明，EA可能对由奥沙利铂引起的神经性疼痛具有明显的镇痛作用，这种疼痛由脊髓胆碱能（M 2 ，M 3 ）和血清素能（5介导）介导。 -HT 3 ）受体。

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