Konno F, Takayanagi I
Jpn J Pharmacol. 1984 Jan;34(1):101-7. doi: 10.1254/jjp.34.101.
We studied the relationship between the inhibition of extracellular 45Ca2+ uptake into synaptosomes and the antinociceptive action induced by morphine, clonidine and papaverine in rats. The antinociceptive action induced by clonidine was as potent as that by morphine, but that by papaverine was less potent than those by morphine and clonidine. Antinociceptive action by morphine was considerably potentiated by the simultaneous administration of clonidine. However, the antinociceptive actions induced by morphine and clonidine were found to be mediated through different receptor mechanisms. Although the pretreatment by papaverine blocked the morphine-induced antinociception, the inhibition induced by papaverine was not found to be mediated through the opiate receptor because papaverine did not displace [3H]-dihydromorphine binding to the membrane fraction from rat brain. Papaverine also inhibited the antinociceptive action induced by clonidine. Morphine inhibited the veratrine-stimulated synaptosomal 45Ca2+ uptake by a naloxone-reversible process. Papaverine also strongly inhibited the veratrine-stimulated synaptosomal 45Ca2+ uptake, while clonidine had virtually no effect. The inhibition of synaptosomal 45Ca2+ uptake induced by morphine was not increased by simultaneous addition of clonidine. The strong inhibitions of synaptosomal 45Ca2+ uptake were still observed by simultaneous addition of papaverine with morphine and clonidine.(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了大鼠体内突触体对细胞外45Ca2+摄取的抑制作用与吗啡、可乐定和罂粟碱诱导的抗伤害感受作用之间的关系。可乐定诱导的抗伤害感受作用与吗啡相当，但罂粟碱诱导的抗伤害感受作用比吗啡和可乐定弱。同时给予可乐定可显著增强吗啡的抗伤害感受作用。然而，发现吗啡和可乐定诱导的抗伤害感受作用是通过不同的受体机制介导的。尽管罂粟碱预处理可阻断吗啡诱导的抗伤害感受作用，但未发现罂粟碱诱导的抑制作用是通过阿片受体介导的，因为罂粟碱不能取代[3H]-二氢吗啡与大鼠脑细胞膜部分的结合。罂粟碱也抑制可乐定诱导的抗伤害感受作用。吗啡通过纳洛酮可逆的过程抑制藜芦碱刺激的突触体45Ca2+摄取。罂粟碱也强烈抑制藜芦碱刺激的突触体45Ca2+摄取，而可乐定几乎没有作用。同时添加可乐定不会增加吗啡诱导的突触体45Ca2+摄取的抑制作用。同时添加罂粟碱与吗啡和可乐定仍可观察到对突触体45Ca2+摄取的强烈抑制作用。（摘要截短至250字）
