Mathematical modelling of delayed calcium deregulation in brain neurons caused by hyperstimulation of glutamate receptors

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...

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Bibliographic Details
Published in:	Biofizika Vol. 59; no. 2; p. 290
Main Authors:	Chastukhin, D S, Borodin, A V, Khodorov, B I
Format:	Journal Article
Language:	Russian
Published:	Russia (Federation) 01-03-2014
Subjects:	Action Potentials Animals Brain - cytology Brain - metabolism Calcium - metabolism Cells, Cultured Membrane Potential, Mitochondrial Models, Neurological Neurons - metabolism Rats Receptors, Glutamate - metabolism
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Summary:	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.
ISSN:	0006-3029