Koizumi S, Ikeda M, Nakazawa K, Inoue K, Nagamatsu K, Hasegawa A, Inoue K
Division of Pharmacology, National Institute of Health Sciences, Tokyo, Japan.
Neurosci Lett. 1995 Jan 2;183(1-2):104-7. doi: 10.1016/0304-3940(94)11125-3.
We previously demonstrated that 5-hydroxytryptamine (5-HT) enhances the cationic current activated by extracellular ATP in rat pheochromocytoma PC12 cells. We report here that pertussis toxin (PTX) modulates this 5-HT-dependent enhancement in these cells. 5-HT potentiated ATP-evoked intracellular Ca2+ concentration ([Ca]i) rise and dopamine release over a concentration range from 1 to 100 microM. When cells were pre-treated with PTX, this potentiation was accentuated. Pretreatment with PTX also accentuated the 5-HT-dependent enhancement of the ATP-activated current. These results suggest that the enhancement by 5-HT of the ATP-evoked responses is negatively regulated by a mechanism mediated through PTX-sensitive GTP-binding protein.
我们先前证明，5-羟色胺（5-HT）可增强大鼠嗜铬细胞瘤PC12细胞中细胞外ATP激活的阳离子电流。我们在此报告，百日咳毒素（PTX）可调节这些细胞中这种5-HT依赖性增强作用。在1至100微摩尔的浓度范围内，5-HT可增强ATP诱发的细胞内Ca2+浓度（[Ca]i）升高和多巴胺释放。当细胞用PTX预处理时，这种增强作用会更加明显。PTX预处理还增强了5-HT对ATP激活电流的依赖性增强作用。这些结果表明，5-HT对ATP诱发反应的增强作用受到一种通过PTX敏感的GTP结合蛋白介导的机制的负调控。
