Ikeuchi Y, Nishizaki T, Mori M, Okada Y
Department of Physiology, Kobe University School of Medicine, Japan.
Biochem Biophys Res Commun. 1996 Jan 17;218(2):428-33. doi: 10.1006/bbrc.1996.0076.
A potent P2Y purinoceptor agonist, 2-methylthio ATP (2-MeSATP), produced whole-cell potassium currents through a purinoceptor linked to a pertussis toxin (PTX)-insensitive G-protein in rat hippocampal neurons. The currents were not affected by a selective protein kinase C or A inhibitor. Single channel recordings demonstrated that the potassium channel is activated without latency even in outside-out patches. These suggest that the channel may be regulated directly by the beta gamma subunits of a G-protein. In addition, 2-MeSATP enhanced intracellular free Ca2+ concentration ([Ca2+]i) with a very rapid initiation time. The [Ca2+]i increase was inhibited by a broad G-protein inhibitor, but not by a phospholipase C (PLC) inhibitor or an IP3 receptor antagonist. These indicate that this Ca2+ mobilization may be regulated by a mechanism independent of a PLC-mediated phosphatidylinositol signaling pathway.
一种强效的P2Y嘌呤受体激动剂，2-甲硫基三磷酸腺苷（2-MeSATP），通过与百日咳毒素（PTX）不敏感的G蛋白相连的嘌呤受体在大鼠海马神经元中产生全细胞钾电流。这些电流不受选择性蛋白激酶C或A抑制剂的影响。单通道记录表明，即使在外翻膜片中，钾通道也能无延迟地被激活。这些表明该通道可能直接由G蛋白的βγ亚基调节。此外，2-MeSATP能以非常快的起始时间提高细胞内游离钙离子浓度（[Ca2+]i）。[Ca2+]i的增加被一种广泛的G蛋白抑制剂抑制，但不受磷脂酶C（PLC）抑制剂或IP3受体拮抗剂的抑制。这些表明这种钙离子动员可能由一种独立于PLC介导的磷脂酰肌醇信号通路的机制调节。
