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细胞质Ca2+振荡在暴露于葡萄糖的胰岛β细胞簇中的传播。

Propagation of cytoplasmic Ca2+ oscillations in clusters of pancreatic beta-cells exposed to glucose.

作者信息

Gylfe E, Grapengiesser E, Hellman B

机构信息

Department of Medical Cell Biology, Uppsala University, Sweden.

出版信息

Cell Calcium. 1991 Feb-Mar;12(2-3):229-40. doi: 10.1016/0143-4160(91)90023-8.

DOI:10.1016/0143-4160(91)90023-8
PMID:2059995
Abstract

Digital image analysis was employed for resolving the temporal and spatial variations of the cytoplasmic Ca2+ concentration ([Ca2+]i) in pancreatic beta-cells loaded with the Ca(2+)-indicator Fura-2. Glucose-stimulated individual beta-cells exhibited large amplitude oscillations of [Ca2+]i with a mean frequency of 0.33 min-1. When Ca2+ diffusion was restricted by increasing the Ca2+ buffering capacity, the sugar-induced rise of [Ca2+]i preferentially affected the peripheral cytoplasm. When glucagon was present glucose also caused less prominent oscillations with about a 10-fold higher frequency superimposed on an elevated [Ca2+]i. In small clusters of 6-14 cells the average frequency of the large amplitude oscillations increased to 0.60 min-1. The clusters were found to contain micro-domains of electrically coupled cells with synchronized oscillations. After increasing the glucose concentration, adjacent domains became functionally coupled. The oscillations originated from different cells in the cluster. Also the fast glucagon-dependent oscillations were synchronized between cells and had different origins. The results indicate that coupling of beta-cells leads to an increased frequency of the large amplitude oscillations, and that the oscillatory characteristics are determined collectively among electrically coupled beta-cells rather than by particular pacemaker cells. In the light of these data it is necessary to reconsider the previous ideas that glucose-induced oscillations of membrane potential and [Ca2+]i require coupling between many beta-cells, and that the peak [Ca2+]i values reached during oscillations should increase with the size of the coupled cluster.

摘要

采用数字图像分析技术来解析负载Ca(2+)指示剂Fura-2的胰腺β细胞中细胞质Ca2+浓度([Ca2+]i)的时空变化。葡萄糖刺激的单个β细胞表现出[Ca2+]i的大幅度振荡,平均频率为0.33 min-1。当通过增加Ca2+缓冲能力来限制Ca2+扩散时,糖诱导的[Ca2+]i升高优先影响外周细胞质。当存在胰高血糖素时,葡萄糖也会引起不太明显的振荡,在升高的[Ca2+]i上叠加约高10倍的频率。在由6 - 14个细胞组成的小细胞簇中,大幅度振荡的平均频率增加到0.60 min-1。发现这些细胞簇包含具有同步振荡的电耦合细胞微区。增加葡萄糖浓度后,相邻微区在功能上耦合。振荡起源于细胞簇中的不同细胞。快速的胰高血糖素依赖性振荡在细胞间也同步且起源不同。结果表明,β细胞的耦合导致大幅度振荡频率增加,并且振荡特性是由电耦合的β细胞集体决定的,而不是由特定的起搏细胞决定。鉴于这些数据,有必要重新考虑以前的观点,即葡萄糖诱导的膜电位和[Ca2+]i振荡需要许多β细胞之间的耦合,并且振荡期间达到的[Ca2+]i峰值应随耦合簇的大小而增加。

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