Mitochondrial Trafficking in Neurons: A Key Variable in Neurodegeneration?
Mitochondrial Trafficking in Neurons: A Key Variable in Neurodegeneration?
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DOI：
10.1023/b:jobb.0000041754.78313.c2
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发表时间：
2004-08
影响因子：
3
通讯作者：
I. Reynolds;L. Malaiyandi;Marcy Coash;G. Rintoul
中科院分区：
文献类型：
--
作者：
I. Reynolds;L. Malaiyandi;Marcy Coash;G. Rintoul
线粒体是许多不同神经毒素的近靶点。通常，通过毒素损害线粒体的关键生物能量功能被认为是主要的作用机制。然而，在神经元中能量产生的有效维持除了传统的生物能量功能之外还依赖于线粒体的生物发生、运输和降解。我们最近已经证明，谷氨酸盐改变了原代神经元中线粒体的运输和形态。此外，其他几种潜在的神经毒素，包括一氧化氮和锌，抑制线粒体运动，在某些情况下，也改变形态。这表明神经毒素的某些作用可能包括神经元中线粒体运输的损伤，从而导致局部ATP递送的失败。
Mitochondria are the proximate target of a number of different neurotoxins. Typically, impairing of the key bioenergetic function of mitochondria by toxins is considered as the main mechanism of action. However, the effective maintenance of energy generation in neurons depends on the biogenesis, trafficking, and degradation of mitochondria in addition to the traditional bioenergetic functions. We have recently demonstrated that glutamate alters both the trafficking and morphology of mitochondria in primary neurons. In addition, several other potential neurotoxins, including nitric oxide and zinc, inhibit mitochondrial movement and, in some cases, alter morphology too. This suggests that some part of the action of neurotoxins might include the impairment of mitochondrial trafficking in neurons, with the resultant failure of local ATP delivery.