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突触处的线粒体钙。

Mitochondrial calcium at the synapse.

机构信息

Tata Institute of Fundamental Research, Hyderabad, India.

Tata Institute of Fundamental Research, Hyderabad, India.

出版信息

Mitochondrion. 2021 Jul;59:135-153. doi: 10.1016/j.mito.2021.04.006. Epub 2021 Apr 23.

Abstract

Mitochondria are dynamic organelles, which serve various purposes, including but not limited to the production of ATP and various metabolites, buffering ions, acting as a signaling hub, etc. In recent years, mitochondria are being seen as the central regulators of cellular growth, development, and death. Since neurons are highly specialized cells with a heavy metabolic demand, it is not surprising that neurons are one of the most mitochondria-rich cells in an animal. At synapses, mitochondrial function and dynamics is tightly regulated by synaptic calcium. Calcium influx during synaptic activity causes increased mitochondrial calcium influx leading to an increased ATP production as well as buffering of synaptic calcium. While increased ATP production is required during synaptic transmission, calcium buffering by mitochondria is crucial to prevent faulty neurotransmission and excitotoxicity. Interestingly, mitochondrial calcium also regulates the mobility of mitochondria within synapses causing mitochondria to halt at the synapse during synaptic transmission. In this review, we summarize the various roles of mitochondrial calcium at the synapse.

摘要

线粒体是具有动态的细胞器,具有多种功能,包括但不限于产生 ATP 和各种代谢物、缓冲离子、充当信号枢纽等。近年来,线粒体被视为细胞生长、发育和死亡的中心调节者。由于神经元是具有高代谢需求的高度特化细胞,因此神经元是动物中拥有最多线粒体的细胞之一也就不足为奇了。在突触处,线粒体的功能和动态受到突触钙的严格调节。突触活动期间钙内流导致线粒体钙内流增加,从而增加 ATP 产生并缓冲突触钙。虽然突触传递过程中需要增加 ATP 产生,但线粒体的钙缓冲对于防止神经传递错误和兴奋毒性至关重要。有趣的是,线粒体钙还调节突触内线粒体的迁移性,使线粒体在突触传递过程中在突触处停止。在这篇综述中,我们总结了线粒体钙在突触处的各种作用。

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