Grubelnik V, Larsen A Z, Kummer U, Olsen L F, Marhl M
Department of Physics, Faculty of Education, University of Maribor, Koroska cesta 160, SI-2000, Maribor, Slovenia
Biophys Chem. 2001 Dec 11;94(1-2):59-74. doi: 10.1016/s0301-4622(01)00211-3.
In a mathematical model for simple calcium oscillations [Biophys. Chem. 71 (1998) 125], it has been shown that mitochondria play an important role in the maintenance of constant amplitudes of cytosolic Ca(2+) oscillations. Simple plausible rate laws for Ca(2+) fluxes across the inner mitochondrial membrane have been used in this model. Here we show that it is possible to use the same rate laws as a plug-in element in other existing mathematical models and obtain the same effect on amplitude regulation. This result appears to be universal, independent of the type of model and the type of Ca(2+) oscillations. We demonstrate this on two models for spiking Ca(2+) oscillations [J. Biol. Chem. 266 (1991) 11068; Cell Calcium 14 (1993) 311] and on two recent models for bursting Ca(2+) oscillations; one of them being a receptor-operated model [Biophys. J. 79 (2000) 1188] and the other one being a store-operated model [BioSystems 57 (2000) 75].
在一个关于简单钙振荡的数学模型中[《生物物理化学》71 (1998) 125]，研究表明线粒体在维持胞质Ca(2+)振荡的恒定振幅方面起着重要作用。该模型中使用了关于Ca(2+)跨线粒体内膜通量的简单合理速率定律。在此我们表明，有可能将相同的速率定律作为一个插件元素应用于其他现有的数学模型中，并在振幅调节方面获得相同的效果。这一结果似乎具有普遍性，与模型类型和Ca(2+)振荡类型无关。我们在两个关于尖峰状Ca(2+)振荡的模型[《生物化学杂志》266 (1991) 11068；《细胞钙》14 (1993) 311]以及两个最近关于爆发性Ca(2+)振荡的模型上证明了这一点；其中一个是受体介导模型[《生物物理杂志》79 (2000) 1188]，另一个是储存库介导模型[《生物系统》57 (2000) 75]。
