Relationship between inhibitory effect of endogenous opioid via mu-receptors and muscarinic autoinhibition in acetylcholine release from myenteric plexus of guinea pig ileum.
Relationship between inhibitory effect of endogenous opioid via mu-receptors and muscarinic autoinhibition in acetylcholine release from myenteric plexus of guinea pig ileum.
复制标题
内源性阿片类药物通过 mu 受体的抑制作用与豚鼠回肠肌间丛释放乙酰胆碱的毒蕈碱自身抑制之间的关系。
DOI：
10.1254/jjp.77.279
复制
发表时间：
1998
期刊：
影响因子：
--
通讯作者：
F. Hata
中科院分区：
文献类型：
--
作者：
H. Nishiwaki;N. Saitoh;H. Nishio;T. Takeuchi;F. Hata
在豚鼠回肠纵行肌间神经丛（LMMP）标本上，研究了阿片受体激活与毒蕈碱自抑制肌间神经丛乙酰胆碱（ACh）释放的关系。μ受体激动剂[D-Ala 2，N-Me-Phe 4，Gly 5-ol]脑啡肽（DAMGO）在1 μ M浓度下抑制1 Hz电场刺激（EFS）诱发的ACh释放，但在10 Hz时不抑制。在用阿托品（1 μ M）阻断毒蕈碱自身受体后，DAMGO也在10 Hz下抑制EFS诱发的ACh释放。在用毒蕈碱（200 μ M）有效激活自身受体后，DAMGO在1Hz的抑制作用被消除。1 μ M的κ受体激动剂U-50，488在1和10 Hz下均抑制EFS诱发的ACh释放。U-50，488抑制ACh释放，无论阿托品或毒蕈碱的存在。δ激动剂脑啡肽[D-PEN 2.5]（PDPDE）未显示任何显著作用。另一方面，选择性μ受体拮抗剂，cyprodime，在1 Hz，但不是在10 Hz的EFS引起的ACh释放增加。在自身受体被阻断后，cyprodime也在10 Hz下增加了EFS诱发的ACh释放。选择性κ-受体拮抗剂，去甲binaltorphimine，不影响乙酰胆碱释放的情况下或存在的阿托品。结果表明，内源性阿片通过激活豚鼠回肠LMMP中的μ受体而非κ受体和δ受体来抑制乙酰胆碱的释放，当毒蕈碱自抑制机制不能完全发挥作用时，内源性阿片对乙酰胆碱释放的抑制作用是重要的。
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 microM 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 microM), DAMGO inhibited EFS-evoked ACh release also at 10 Hz. After the autoreceptors were potently activated with muscarine (200 microM), the inhibitory effect of DAMGO at 1 Hz was abolished. A kappa-receptor agonist, U-50,488, at 1 microM 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.
DOI：
10.1073/pnas.84.15.5487
发表时间：
1987-08-01
影响因子：
11.1
作者：
NORTH, RA;WILLIAMS, JT;CHRISTIE, MJ
通讯作者：
CHRISTIE, MJ