Changes in mitochondrial NAD(P)H and glutamate-induced delayed calcium deregulation in cultured rat cerebellar granule neurons

被引:1
作者
Surin A.M. [1 ]
Zobova S.N. [1 ,3 ]
Tukhbatova G.R. [2 ]
Senilova Y.E. [2 ]
Pinelis V.G. [2 ]
Khodorov B.I. [1 ]
机构
[1] Institute of General Pathology and Patophysiology, Russian Academy of Medical Sciences, Moscow 125315, Baltiyskaya ul.
[2] Scientific Centre for Children Health, Russian Academy of Medical Sciences, Moscow 119911, Lomonosovsky prosp.
[3] Voyno-Yasenetsky Krasnoyarsk State Medical University, Krasnoyarsk 660022, Partizan Zheleznyak ul.
基金
俄罗斯基础研究基金会;
关键词
Delayed calcium deregulation; Glutamate; Mitochondria; NAD(P)H; Neurons;
D O I
10.1134/S1990747810010058
中图分类号
学科分类号
摘要
Changes in cytosolic [Ca2+]i, mitochondrial potential (ΔVm), and mitochondrial NAD(P)H autofluorescence were compared in experiments on cultured cerebellar granule cells co-loaded with Ca2+ indicator Fluo-3FF or mitochondrial potential-sensitive probe Rh123. In the majority of neurons (94% of cells, n = 205, 28 experiments) the delayed Ca 2+ deregulation (DCD) induced by Glu (100 μM) was preceded by more or less prolonged decrease in NAD(P)H, which in 57% of cells underwent a further (secondary) reduction during DCD development. To clarify the origin of these changes in NAD(P)H production during DCD we examined the effects of the protonophore FCCP on NAD(P)H increase induced by the electron chain blocker CN (3 mM) application. The data suggest that a pronounced lowering of mitochondrial pH during DCD contributed to the mechanism of Glu-induced suppression of NAD(P)H production. © 2010 Pleiades Publishing, Ltd.
引用
收藏
页码:32 / 37
页数:5
相关论文
共 14 条
  • [11] Wang G.J., Randall R.D., Thayer S.A., Glutamate-induced intracellular acidification of cultured hippocampal neurons demonstrates altered energy metabolism resulting from ca<sup>2+</sup> loads, J. Neurophysiol., 72, pp. 2563-2569, (1994)
  • [12] Kiedrowski L., N-methyl-D-aspartate excitotoxicity: relationships among plasma membrane potential, Na+/Ca<sup>2+</sup> exchange, mitochondrial Ca<sup>2+</sup> overload, and cytoplasmic concentrations of Ca<sup>2+</sup>, H+, and K<sup>+</sup>, Mol. Pharmacol., 56, pp. 619-632, (1999)
  • [13] Bolshakov A.P., Mikhailova M.M., Szabadkai G., Pinelis V.G., Brustovetsky N., Rizzuto R., Khodorov B.I., Measurements of mitochondrial ph in cultured cortical neurons clarify contribution of mitochondrial pore to the mechanism of glutamate-induced delayed ca<sup>2+</sup> deregulation, Cell Calcium, 43, pp. 602-614, (2008)
  • [14] Surin A.M., Bolshakov A.P., Mikhailova M.M., Motin V.G., Storozhevykh T.P., Pinelis V.G., Khodorov B.I., Khiroug L.S., Intracellular calcium and ph changes in cultured neurons during glutamate challenge and post-glutamate period, Internationl Conference Receptors and Intracellular Signaling, pp. 100-102, (2007)