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首页> 外文期刊>Japanese Journal of Pharmacology >Relationship Between Inhibitory Effect of Endogenous Opioid via Mu-Receptors and Muscarinic Autoinhibition in Acetylcholine Release From Myenteric Plexus of Guinea Pig Ileum
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Relationship Between Inhibitory Effect of Endogenous Opioid via Mu-Receptors and Muscarinic Autoinhibition in Acetylcholine Release From Myenteric Plexus of Guinea Pig Ileum

机译：内源性阿片样物质通过Mu受体抑制作用与毒蕈碱自抑制对豚鼠回肠中枢神经丛释放乙酰胆碱的关系

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References(34) Cited-By(10) Relationship between activation of opioid receptors and muscarinic autoinhibition in acetylcholine (ACh) release from the myenteric plexus was studied in longitudinal muscle myenteric plexus (LMMP) preparations of guinea pig ileum. A mu-receptor agonist, [D-Ala2, N-Me-Phe4, Gly5-ol] enkephalin (DAMGO), at a concentration of 1 μM inhibited the ACh release evoked by electrical field stimulation (EFS) at 1 Hz but not at 10 Hz. After the muscarinic autoreceptors were blocked with atropine (1 μM), DAMGO inhibited EFS-evoked ACh release also at 10 Hz. After the autoreceptors were potently activated with muscarine (200 μM), the inhibitory effect of DAMGO at 1 Hz was abolished. A kappa-receptor agonist, U-50, 488, at 1 μM inhibited the EFS-evoked ACh release both at 1 and 10 Hz. U-50, 488 inhibited ACh release regardless of the presence of atropine or muscarine. A delta-agonist, enkephalin [D-PEN2.5] (PDPDE), did not show any significant effect. On the other hand, a selective mu-receptor antagonist, cyprodime, increased ACh release evoked by EFS at 1 Hz, but not at 10 Hz. After the autoreceptors were blocked, cyprodime increased EFS-evoked ACh release also at 10 Hz. The selective kappa-receptor antagonist, nor-binaltorphimine, did not affect ACh release in the absence or presence of atropine. The results suggest that endogenous opioid(s) inhibits ACh release by activating mu-, but not kappa- and delta-receptors in the LMMP of guinea pig ileum and that the inhibitory effect of endogenous opioid(s) in the ACh release is important when muscarinic autoinhibition mechanism does not fully work.
机译：参考文献（34）引用了（10）在豚鼠回肠的纵向肌肉肌层神经丛（LMMP）制剂中研究了阿片样物质受体的激活与从肌层神经丛释放的乙酰胆碱（ACh）中毒蕈碱自身抑制之间的关系。浓度为1μM的mu受体激动剂[D-Ala2，N-Me-Phe4，Gly5-ol]脑啡肽（DAMGO）在1 Hz时抑制了电场刺激（EFS）引起的ACh释放，但在1 Hz时却没有。 10赫兹在毒蕈碱自身受体被阿托品（1μM）阻断后，DAMGO在10 Hz时也抑制EFS诱发的ACh释放。在自动受体被毒蕈碱（200μM）有效激活后，DAMGO在1 Hz时的抑制作用被取消。 1μM的κ受体激动剂U-50、488抑制1和10 Hz时EFS诱发的ACh释放。 U-50、488抑制ACh的释放，而不管阿托品或毒蕈碱的存在。 δ-激动剂脑啡肽[D-PEN2.5]（PDPDE）没有显示任何明显的作用。另一方面，选择性mu受体拮抗剂cyprodime在1 Hz而不是10 Hz时增加了EFS引起的ACh释放。阻断自身受体后，环丙啶在10 Hz时也会增加EFS诱发的ACh释放。在阿托品不存在或不存在的情况下，选择性κ受体拮抗剂也不是去甲萘酚明不影响ACh的释放。结果表明，内源性阿片类药物通过激活豚鼠回肠LMMP中的mu受体而不是κ和δ受体来抑制ACh的释放，内源性阿片类药物对ACh释放的抑制作用很重要。毒蕈碱自抑制机制不能完全起作用。

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