Mihara S, North R A
Br J Pharmacol. 1986 Jun;88(2):315-22. doi: 10.1111/j.1476-5381.1986.tb10207.x.
Intracellular records were made from neurones in the submucous plexus of the guinea-pig caecum. [Met5]enkephalin, [Leu5]enkephalin, [D-Ala2,D-Leu5]enkephalin (DADLE) and [D-Ser2,Leu5]enkephalin-Thr (DSLET) hyperpolarized the membrane when applied in concentrations of 30 nm-10 microM. Normorphine, [D-Ala2, MePhe4,Gly5]enkephalin-ol (DAGO), [D-Ala2,MePhe4,Met(0)5]enkephalin-ol (FK33824), dynorphin A and tifluadom had no effect at concentrations up to 10 microM. The hyperpolarization resulted from an increase in the membrane potassium conductance. Hyperpolarizations induced by [Met5]enkephalin were antagonized competitively by naloxone and by N-bisallyl[aminoisobutyrate2,3, Leu5]enkephalin (ICI 174864). The Schild plots for these antagonisms had slopes not different from one, and the dissociation equilibrium constants among individual neurones were 5-50 nM for naloxone and 5-60 nM for ICI 174864. The results indicate that the opioid receptors on guinea-pig submucous neurones which are coupled to potassium channels are of the delta-type.
从豚鼠盲肠黏膜下神经丛的神经元进行细胞内记录。[Met5]脑啡肽、[Leu5]脑啡肽、[D - Ala2,D - Leu5]脑啡肽(DADLE)和[D - Ser2,Leu5]脑啡肽 - Thr(DSLET)在浓度为30 nM - 10 μM时可使细胞膜超极化。去甲吗啡、[D - Ala2,MePhe4,Gly5]脑啡肽醇(DAGO)、[D - Ala2,MePhe4,Met(0)5]脑啡肽醇(FK33824)、强啡肽A和替氟朵在浓度高达10 μM时无作用。超极化是由膜钾电导增加所致。[Met5]脑啡肽诱导的超极化可被纳洛酮和N - 双烯丙基[氨基异丁酸2,3,Leu5]脑啡肽(ICI 174864)竞争性拮抗。这些拮抗作用的Schild图斜率与1无差异,单个神经元中纳洛酮的解离平衡常数为5 - 50 nM,ICI 174864为5 - 60 nM。结果表明,豚鼠黏膜下神经元上与钾通道偶联的阿片受体为δ型。