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受体激活的细胞质Ca2+峰值由内醇三酸介导,是由于Ca2(+) 诱导的Ca2+释放

M Wakui¹, Y V Osipchuk, O H Petersen

¹MRC Secretory Control Research Group, University of Liverpool, England.

|November 30, 1990

概括

乙胆通过对咖啡因敏感的道触发胰腺细胞中的振荡. 这一过程涉及因诺西1,4,5-三酸盐 (Ins(1,4,5) P3) 介导的释放,与直接输液效应不同.

科学领域:

细胞生理学细胞生理学
信号传递信号传递
胃肠道生理学胃肠道生理学

背景情况:

受体介导的信号通路控制细胞内 (Ca2+) 的动态.
伊诺西1,4,5-三酸盐 (Ins(1,4,5) P3) 的生成导致Ca2+的释放和振荡.
胰腺小细胞利用Ca2+信号进行分泌.

研究的目的:

阐明胰腺小细胞中由乙胆 (ACh) 引起的Ca2+振荡背后的机制.
为了区分Ins(1,4,5) P3受体和Ca2+诱导的Ca2+释放 (CICR) 在Ca2+信号传递中的作用.
研究咖啡因敏感通道对Ca2+释放的贡献.

主要方法:

补丁电生理学监测Ca2+激活的Cl-电流.
细胞内Ca2+和Ins(1,4,5) P3输入到单个小鼠胰腺状细胞中.
乙胆 (ACh),Ins{1,4,5) P3,肝素和咖啡因的应用.

主要成果:

细胞内Ca2+输液模仿了ACh/Ins{1,4,5) P3效应,导致Ca2+释放.
肝素是一种Ins{1,4,5) P3受体对抗剂,阻断了ACh/Ins{1,4,5) P3振荡,但没有Ca2+输液诱导的升.
咖啡因在小于值的Ca2+输液中强化了Ca2+的升,这表明CICR的作用.

结论:

由ACh引起的Ca2+振荡取决于通过咖啡因敏感通道释放的Ca2+脉冲.
一个小而稳定的Ins(1,4,5) P3引起的Ca2+流动触发了这些脉冲.
该机制不同于仅由Ins{1,4,5) P3受体介导的Ca2+释放或直接的Ca2+输注.

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