摘要
Calcium is a ubiquitous second messenger. Mitochondria contributes significantly to intracellular Ca^2＋ dynamics. The experiment of Kaftan et al. [J. Biol. Chem. 275（2000） 25465] demonstrated that inhibiting mitochondrial Ca^2＋ uptake can reduce the frequency of cytosolic Ca^2＋ concentration oscillations of gonadotropes. By considering the mitochondrial Ca^2＋ cycling we develop a three-variable model of intracellular Ca^2＋ oscillations based on the models of Atri et al. [Biophys. J. 65 （1993） 1727] and Falcke et al. [Biophys. J. 77 （1999） 37]. The model reproduces the fact that mitochondrial Ca^2＋ cycling increases the frequency of cytosolic Ca^2＋ oscillations, which accords with Kaftan＇s results. Moreover the model predicts that when the mitochondria overload with Ca^2＋, the cytosolic Ca^2＋ oscillations vanish, which may trigger apoptosis.
Calcium is a ubiquitous second messenger. Mitochondria contributes significantly to intracellular Ca^2＋ dynamics. The experiment of Kaftan et al. [J. Biol. Chem. 275（2000） 25465] demonstrated that inhibiting mitochondrial Ca^2＋ uptake can reduce the frequency of cytosolic Ca^2＋ concentration oscillations of gonadotropes. By considering the mitochondrial Ca^2＋ cycling we develop a three-variable model of intracellular Ca^2＋ oscillations based on the models of Atri et al. [Biophys. J. 65 （1993） 1727] and Falcke et al. [Biophys. J. 77 （1999） 37]. The model reproduces the fact that mitochondrial Ca^2＋ cycling increases the frequency of cytosolic Ca^2＋ oscillations, which accords with Kaftan＇s results. Moreover the model predicts that when the mitochondria overload with Ca^2＋, the cytosolic Ca^2＋ oscillations vanish, which may trigger apoptosis.
