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Mechanisms of cytosolic Ca^<2+> oscillations following muscarinic receptor activation in single smooth muscle cells

单平滑肌细胞毒蕈碱受体激活后胞质Ca^2振荡的机制

基本信息

批准号：
06660377
负责人：
KOMORI Seiichi
金额：
$ 0.19万
依托单位：
Gifu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06660377/
关键词：
Smooth muscle Muscarinic receptor Calcium release Calcium store Calcium oscillations Inositol trisphosphate G protein Patch clamp ライアナジン

项目摘要

The present study was made to elucidate the underlying mechanism of oscillations in cytosolic calcium concentration ([Ca^<2+>]i) following activation of muscarinic receptors in single smooth muscle cells of guinea-pig ileum, in an attempt to provide some insights into functional roles of [Ca^<2+>]i oscillations. Changes in [Ca^<2+>]i were measured directly using a Ca^<2+>-sensitive dye or indirectly by recording [Ca^<2+>]i-dependent ionic currents by the patch clamp technique.1.Muscarinic agonist-induced [Ca^<2+>]i oscillations occur as a result of periodic release of Ca^<2+> from internal Ca^<2+> stores. The same mechanism can be operated to induce [Ca^<2+>]i oscillations after activation of G proteins by GTPgammaS.2.Inositol 1,4,5-trisphosphate (InsP3) functions as a Ca^<2+>-releasing second messenger for generation of muscarinic [Ca^<2+>]i oscillations.3.Ca^<2+>-releasing action of InsP3 is inhibited by a rise of [Ca^<2+>]i to a certain level, and loss of the inhibition with falling [Ca^<2+>]i and with time allows InsP3 to act. This [Ca^<2+>]i-dependent inhibition of InsP3 action may contribute to periodic Ca^<2+> release from the stores during muscarinic receptor activation.4.Ca^<2+> influx across the plasma membrane has a crutial role to play in regulation of the frequency of [Ca^<2+>]i oscillations, and the effect is brought about through a mechanism independent of Ca^<2+> store replenishment. The voltage-gated Ca^<2+> channel and an as yet unidentified channel are both involved in Ca^<2+> entry responsible for modulation of [Ca^<2+>]i oscillations.5.Ca^<2+> stores have a Ca^<2+>-induced Ca^<2+> release mechanism in addition to the Ins-P3 induced Ca^<2+> release mechanism, but the former mechanism may little contribute to the generation of muscarinic [Ca^<2+>]i oscillations.

本研究旨在阐明豚鼠回肠平滑肌细胞M受体激活后胞浆内钙离子浓度（[Ca^2+]i）振荡的机制，试图为[Ca^2+]i振荡的功能作用提供一些见解。[Ca^<2+>]i的变化用Ca^<2+>敏感染料直接测量或用膜片钳技术记录[Ca^<2+>] i依赖性离子电流间接测量。1.毒蕈碱激动剂诱导的[Ca^<2+]i振荡是由于细胞内Ca ^<2 +>库周期性释放Ca^<2+的结果。3.[Ca ^2 +]i升高到一定水平时，InsP 3的释放Ca^2+的作用被抑制，[Ca^2 +] i的释放被抑制，[Ca^2 +]i的释放被抑制，[Ca^2+]i的释放被抑制，[Ca^2+] i的释放被抑制。随着[Ca^2+]i的降低和时间的延长，抑制作用的丧失使InsP 3能够发挥作用。这种依赖于[Ca^<2+>] i的InsP 3抑制作用可能与M受体激活时钙库的周期性释放有关。4.跨膜Ca^<2 +>内流在调节[Ca^<2+>]i振荡频率中起重要作用，这种作用是通过一种不依赖于Ca^<2+>库补充的机制实现的。电压门控Ca^<2+>通道和一个尚未鉴定的通道都参与了Ca^<2+>内流，负责调节[Ca^<2+>]i振荡。5. Ca ^<2+>库除了具有Ins-P3诱导的Ca ^<2 +>释放机制外，还具有Ca^<2 +>诱导的Ca^<2 +>释放机制，但前者可能对毒蕈碱型[Ca^2+]i振荡的产生贡献不大。