Buchholz Björn, Tauber Robert, Steffl Daniel, Walz Gerd, Köttgen Michael
Renal Division and Center for Clinical Research, University Hospital Freiburg, Breisacherstr. 66, 79106 Freiburg, Germany.
Biochem Biophys Res Commun. 2004 Sep 10;322(1):177-85. doi: 10.1016/j.bbrc.2004.07.103.
Ca(2+) influx across the plasma membrane after stimulation of G protein-coupled receptors is important for many physiological functions. Here we studied the regulation of an inwardly rectifying whole cell current and its putative role in Ca(2+) entry in Xenopus oocytes. Expression of P2Y(1) or M1 receptors in Xenopus oocytes elicited a characteristic inwardly rectifying current without receptor stimulation. This current displayed distinct activation and inactivation kinetics and was highly Ca(2+)-dependent. After stimulation of endogenous G(q)-coupled receptors in water-injected cells similar currents were observed. We therefore speculated that the current could be activated via Ca(2+) store depletion induced by constitutive stimulation of the IP(3) cascade in cells overexpressing G(q)-coupled receptors. Receptor-independent Ca(2+) store depletion also induced the current. In conclusion, this current is activated after store depletion suggesting a role in Ca(2+) entry after stimulation of G(q)-coupled receptors. Finally, our data do not support the proposed ionotropic properties of the P2Y(1) receptor.
G蛋白偶联受体受刺激后，钙离子经质膜内流对许多生理功能都很重要。在此，我们研究了非洲爪蟾卵母细胞内向整流全细胞电流的调节及其在钙离子内流中的假定作用。非洲爪蟾卵母细胞中P2Y(1)或M1受体的表达在无受体刺激时引发了特征性的内向整流电流。该电流表现出独特的激活和失活动力学，且高度依赖钙离子。在注射水的细胞中刺激内源性G(q)偶联受体后，观察到了类似的电流。因此，我们推测该电流可能通过过表达G(q)偶联受体的细胞中IP(3)级联的组成性刺激诱导的钙离子库耗竭而被激活。不依赖受体的钙离子库耗竭也诱导了该电流。总之，该电流在钙离子库耗竭后被激活，提示其在G(q)偶联受体受刺激后的钙离子内流中发挥作用。最后，我们的数据不支持所提出的P2Y(1)受体的离子otropic特性。 （注：原文中“ionotropic”可能有误，推测应为“ionotropic”，意为“离子otropic的” ，这里按推测翻译为“离子otropic特性” ，实际可能需结合更准确的专业知识进一步确认。）
