Mechanisms and roles of mitochondrial localisation and dynamics in neuronal function.

Q4 Neuroscience
Richard Seager, Laura Lee, Jeremy M Henley, Kevin A Wilkinson
{"title":"Mechanisms and roles of mitochondrial localisation and dynamics in neuronal function.","authors":"Richard Seager,&nbsp;Laura Lee,&nbsp;Jeremy M Henley,&nbsp;Kevin A Wilkinson","doi":"10.1042/NS20200008","DOIUrl":null,"url":null,"abstract":"<p><p>Neurons are highly polarised, complex and incredibly energy intensive cells, and their demand for ATP during neuronal transmission is primarily met by oxidative phosphorylation by mitochondria. Thus, maintaining the health and efficient function of mitochondria is vital for neuronal integrity, viability and synaptic activity. Mitochondria do not exist in isolation, but constantly undergo cycles of fusion and fission, and are actively transported around the neuron to sites of high energy demand. Intriguingly, axonal and dendritic mitochondria exhibit different morphologies. In axons mitochondria are small and sparse whereas in dendrites they are larger and more densely packed. The transport mechanisms and mitochondrial dynamics that underlie these differences, and their functional implications, have been the focus of concerted investigation. Moreover, it is now clear that deficiencies in mitochondrial dynamics can be a primary factor in many neurodegenerative diseases. Here, we review the role that mitochondrial dynamics play in neuronal function, how these processes support synaptic transmission and how mitochondrial dysfunction is implicated in neurodegenerative disease.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"4 2","pages":"NS20200008"},"PeriodicalIF":0.0000,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373250/pdf/","citationCount":"50","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuronal signaling","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1042/NS20200008","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Neuroscience","Score":null,"Total":0}
引用次数: 50

Abstract

Neurons are highly polarised, complex and incredibly energy intensive cells, and their demand for ATP during neuronal transmission is primarily met by oxidative phosphorylation by mitochondria. Thus, maintaining the health and efficient function of mitochondria is vital for neuronal integrity, viability and synaptic activity. Mitochondria do not exist in isolation, but constantly undergo cycles of fusion and fission, and are actively transported around the neuron to sites of high energy demand. Intriguingly, axonal and dendritic mitochondria exhibit different morphologies. In axons mitochondria are small and sparse whereas in dendrites they are larger and more densely packed. The transport mechanisms and mitochondrial dynamics that underlie these differences, and their functional implications, have been the focus of concerted investigation. Moreover, it is now clear that deficiencies in mitochondrial dynamics can be a primary factor in many neurodegenerative diseases. Here, we review the role that mitochondrial dynamics play in neuronal function, how these processes support synaptic transmission and how mitochondrial dysfunction is implicated in neurodegenerative disease.

Abstract Image

Abstract Image

Abstract Image

线粒体定位和神经元功能动力学的机制和作用。
神经元是高度极化、复杂且能量密集的细胞,其在神经元传递过程中对ATP的需求主要通过线粒体的氧化磷酸化来满足。因此,维持线粒体的健康和有效功能对神经元的完整性、活力和突触活性至关重要。线粒体不是孤立存在的,而是不断地经历融合和裂变的循环,并主动地在神经元周围运输到高能量需求的部位。有趣的是,轴突和树突状线粒体表现出不同的形态。轴突中的线粒体小而稀疏,而树突中的线粒体大而密集。这些差异背后的运输机制和线粒体动力学,以及它们的功能含义,一直是协同调查的重点。此外,现在很清楚,线粒体动力学缺陷可能是许多神经退行性疾病的主要因素。在这里,我们回顾了线粒体动力学在神经元功能中的作用,这些过程如何支持突触传递以及线粒体功能障碍如何与神经退行性疾病有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
4.60
自引率
0.00%
发文量
0
审稿时长
14 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信