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突触处的线粒体。

Mitochondria at the synapse.

作者信息

Ly Cindy V, Verstreken Patrik

机构信息

Department of Neuroscience and Molecular and Human Genetics, Howard Hughes Medical Institute Baylor College of Medicine, Houston, TX 77030, USA.

出版信息

Neuroscientist. 2006 Aug;12(4):291-9. doi: 10.1177/1073858406287661.

DOI:10.1177/1073858406287661
PMID:16840705
Abstract

Synapses are packed with mitochondria, complex organelles with roles in energy metabolism, cell signaling, and calcium homeostasis. However, the precise mechanisms by which mitochondria influence neurotrans mission remain undefined. In this review, the authors discuss pharmacological and genetic analyses of synaptic mitochondrial function, focusing on their role in Ca2+ buffering and ATP production. Additionally, they will summarize recent data that implicate synaptic mitochondria in the regulation of neurotransmitter release during intense neuronal activity and link these findings to the pathogenesis of neurodegenerative diseases that feature disrupted synaptic mitochondria, including amyotrophic lateral sclerosis and hereditary spastic paraplegia.

摘要

突触中充满了线粒体,线粒体是复杂的细胞器,在能量代谢、细胞信号传导和钙稳态中发挥作用。然而,线粒体影响神经传递的确切机制仍不清楚。在这篇综述中,作者讨论了突触线粒体功能的药理学和遗传学分析,重点关注它们在钙离子缓冲和三磷酸腺苷(ATP)生成中的作用。此外,他们将总结最近的数据,这些数据表明突触线粒体在强烈神经元活动期间对神经递质释放的调节中起作用,并将这些发现与神经退行性疾病的发病机制联系起来,这些疾病的特征是突触线粒体功能紊乱,包括肌萎缩侧索硬化症和遗传性痉挛性截瘫。

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