Nitric oxide mediates glutamate induced mitochondrial depolarization in rat cortical neurons
Nitric oxide mediates glutamate induced mitochondrial depolarization in rat cortical neurons
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DOI：
10.1016/s0006-8993(98)01240-2
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发表时间：
1999-01-23
期刊：
影响因子：
2.9
通讯作者：
Medina, JM
中科院分区：
文献类型：
--
作者：
Almeida, A;Bolaños, JP;Medina, JM
线粒体被认为是谷氨酸神经毒性的靶点。本工作的目的是研究导致谷氨酸介导的线粒体脱髓鞘的机制，通过线粒体膜电位和细胞呼吸在培养的神经元中测量。谷氨酸暴露于细胞诱导明显的线粒体去极化与神经元呼吸损伤，导致神经元ATP耗竭。一氧化氮（NO）-N-.合成酶抑制剂N-ω-硝基-L-精氨酸甲酯和N-甲基-D-天冬氨酸谷氨酸受体亚型抑制剂D-（-）-2氨基-5-磷酸戊酸我们的结果表明谷氨酸通过（NO）-N-.中介机制。(C)1999 Elsevier Science B. V.保留所有权利。
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.