Mitochondrial Lipid Pore in the Mechanism of Glutamate-induced Calcium Deregulation of Neuronsстатья

Информация о цитировании статьи получена из Scopus, Web of Science
Статья опубликована в журнале из перечня ВАК
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 24 октября 2016 г.

Работа с статьей

[1] Mitochondrial lipid pore in the mechanism of glutamate-induced calcium deregulation of neurons / G. D. Mironova, K. N. Belosludtsev, A. M. Surin et al. // Biologicheskie Membrany. — 2011. — Vol. 28, no. 6. — P. 483–494. The work examines the mechanisms of central nerve cell death upon stimulation of brain NMDA receptors with the stimulatory mediator glutamate. A prolonged stimulation of neurons with glutamate is known to result in the disorder of Ca2+ homeostasis and severe mitochondrial depolarization followed by cell death. It has been shown that the overload of mitochondria with Sr2+ leads to the release of the cation, alkalinization of the medium, decrease of membrane potential, and swelling of mitochondria, indicating a nonspecific permeabilization of the mitochondrial membrane. In our opinion, the observed permeabilization is caused by the activation of Ca2+/Sr2+-dependent phospholipase A(2)(PLA(2)), resulting in the formation of free palmitic and stearic acids in the mitochondrial membrane. These fatty acids bind Ca2+ with high affinity, and the binding process is accompanied by the formation of a transient lipid pore a phenomenon demonstrated earlier on both artificial and mitochondrial membranes. The inhibitors of PLA(2) have been shown to suppress permeabilization of mitochondrial membranes. In the culture of cerebellum granular neurons, the PLA(2) inhibitors prolonged the lag of the delayed Sr2+ deregulation and membrane depolarization. Based on these data obtained on isolated mitochondria and neurons we suppose that the initial stages of glutamate-induced Ca2+ deregulation of neurons are underlain by the opening of lipid pores in brain mitochondria.

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