Modeling of the modulation by buffers of Ca2+ release through clusters of IP3 receptors.

Modeling of the modulation by buffers of Ca2+ release through clusters of IP3 receptors.
复制标题

DOI:
10.1016/j.bpj.2009.05.050
复制
发表时间:
2009-08
影响因子:
3.4
通讯作者:
S. Zeller;Sten Rüdiger;Harald Engel;J. Sneyd;Gerald Warnecke;Ian Parker;Martin Falcke
S. Zeller;Sten Rüdiger;Harald Engel;J. Sneyd;Gerald Warnecke;Ian Parker;Martin Falcke
中科院分区:
生物学3区
文献类型:
--
作者:
S. Zeller;Sten Rüdiger;Harald Engel;J. Sneyd;Gerald Warnecke;Ian Parker;Martin Falcke

文献摘要

被引文献

相似文献

细胞内Ca ~(2+)释放是一种多功能的第二信使系统。它是仿照这里的反应扩散方程的游离Ca 2+和Ca 2+缓冲液,空间离散集群随机IP 3受体通道(IP 3Rs)控制释放的Ca 2+从内质网。IP 3R被激活的胞质Ca 2+浓度的小上升和抑制大浓度。胞质Ca 2+的缓冲作用塑造了整体Ca 2+瞬变。在这里,我们使用一个模型来研究具有慢和快反应速率的缓冲液对单个释放尖峰的影响。我们发现,根据其扩散系数,快速缓冲区可以解耦集群或延迟抑制。慢缓冲液对Ca 2+释放的影响很小,但主要通过竞争Ca 2+来影响来自荧光Ca 2+指示剂的信号的时间过程。在低[IP 3]下,快速缓冲液抑制荧光信号,慢速缓冲液增加本体信号和开放簇处的信号之间的对比度,并且大浓度的缓冲液(快速或慢速)使簇去耦。
Intracellular Ca2+release is a versatile second messenger system. It is modeled here by reaction-diffusion equations for the free Ca2+and Ca2+buffers, with spatially discrete clusters of stochastic IP3receptor channels (IP3Rs) controlling the release of Ca2+from the endoplasmic reticulum. IP3Rs are activated by a small rise of the cytosolic Ca2+concentration and inhibited by large concentrations. Buffering of cytosolic Ca2+shapes global Ca2+transients. Here we use a model to investigate the effect of buffers with slow and fast reaction rates on single release spikes. We find that, depending on their diffusion coefficient, fast buffers can either decouple clusters or delay inhibition. Slow buffers have little effect on Ca2+release, but affect the time course of the signals from the fluorescent Ca2+indicator mainly by competing for Ca2+. At low [IP3], fast buffers suppress fluorescence signals, slow buffers increase the contrast between bulk signals and signals at open clusters, and large concentrations of buffers, either fast or slow, decouple clusters.