RESUMO
Mathematical model presented in this paper is based on the data obtained in experimental studies of the mechanism of glutamate-induced deregulation of Ca2+ homeostasis and mitochondrial depolarization in cultured nerve cells. According to our hypothesis the secondary Ca2+ increase during a prolonged glutamate challenge is mainly due to a profound mitochondrial depolarization which stops mitochondrial Ca2+ uptake in the face of continuous Ca2+ influx into the cell. It is supposed that a progressive decrease in mitochondrial NADH during glutamate exposure greatly enhances sensitivity of mitochondria to intracellular Ca-neurotoxicity. A system of equations developed in this work made it possible to provide a satisfactory simulation of most of experimental events observed in the present study.
