Honoré E, Fournier F, Collin T, Nargeot J, Guilbault P
Laboratorie de Physiologie Cellulaire UFR de Biologie, Université des Sciences et Techniques de Lille-Flandres-Artois, Villeneuve d'Ascq, France.
Pflugers Arch. 1991 Jun;418(5):447-52. doi: 10.1007/BF00497772.
Xenopus oocytes injected with embryonic guinea-pig brain mRNA expressed functional P2Y purinoceptors. Extracellular ATP stimulated in a dose-dependent manner a delayed Ca(2+)-dependent Cl- current component. Analysis of the interactions of ATP with compounds that affect Ca2+ fluxes through the plasma membrane or Ca2+ release from internal stores indicates that ATP raises [Ca2+]i by a mechanism that involves activation of voltage-dependent Ca2+ channels, which leads to influx of extracellular Ca2+ into the cells, as well as release of Ca2+ from intracellular stores. Since this phenomenon was not found in control oocytes, it is suggested that brain mRNA encoded for a newly synthesized Ca(2+)-release process stimulated by purinoceptor activation. This mechanism could be largely involved in the short-term regulation of intracellular Ca2+ level involved in ATP neuromodulation functions.
注射了胚胎豚鼠脑信使核糖核酸（mRNA）的非洲爪蟾卵母细胞表达了功能性P2Y嘌呤受体。细胞外三磷酸腺苷（ATP）以剂量依赖的方式刺激了一种延迟的、依赖钙离子（Ca(2+)）的氯离子电流成分。对ATP与影响钙离子通过质膜通量或从内部储存库释放钙离子的化合物之间相互作用的分析表明，ATP通过一种机制提高细胞内钙离子浓度（[Ca2+]i），该机制涉及电压依赖性钙离子通道的激活，这导致细胞外钙离子流入细胞，以及细胞内储存库释放钙离子。由于在对照卵母细胞中未发现这种现象，因此提示脑信使核糖核酸编码了一种由嘌呤受体激活所刺激的新合成的钙离子释放过程。这种机制可能在很大程度上参与了与ATP神经调节功能相关的细胞内钙离子水平的短期调节。
