Nitric oxide mediates glutamate induced mitochondrial depolarization in rat cortical neurons

被引：43

作者：

Almeida, A ^{[1
]}

Bolaños, JP ^{[1
]}

Medina, JM ^{[1
]}

机构：

[1] Univ Salamanca, Fac Farm, Dept Bioquim & Biol Mol, Edificio Dept, E-37007 Salamanca, Spain

来源：

BRAIN RESEARCH | 1999年 / 816卷 / 02期

关键词：

glutamate; neurotoxicity; mitochondrial depolarization; rhodamine; 123; neurons;

D O I：

10.1016/S0006-8993(98)01240-2

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Mitochondria have been considered to be a target for glutamate neurotoxicity. The aim of the present work was to investigate the mechanisms leading to glutamate-mediated mitochondrial deenergization, as measured by mitochondrial membrane potential and cell respiration in cultured neurons. Glutamate exposure to cells induced pronounced mitochondrial depolarization associated with an impairment in neuronal respiration, leading to neuronal ATP depletion. These effects were prevented by both the nitric oxide ((NO)-N-.) synthase inhibitor N-omega-nitro-L-arginine methyl ester and by the N-methyl-D-aspartate glutamate-subtype receptor inhibitor D-(-)-2amino-5-phosphopentanoate Our results suggest that glutamate causes ATP depletion by collapsing mitochondrial membrane potential through a (NO)-N-.-mediated mechanism. (C) 1999 Elsevier Science B.V. All rights reserved.

引用

页码：580 / 586

页数：7

共 27 条

[1] HYPOTHYROIDISM PREVENTS POSTNATAL CHANGES IN RAT-LIVER MITOCHONDRIAL POPULATIONS DEFINED BY RHODAMINE-123 STAINING [J].