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突触处的自噬。

Autophagy at the synapse.

作者信息

Birdsall Veronica, Waites Clarissa L

机构信息

Neurobiology and Behavior Graduate Program, Columbia University, United States.

Department of Pathology & Cell Biology, Columbia University Medical Center, United States; Department of Neuroscience, Columbia University, United States.

出版信息

Neurosci Lett. 2019 Apr 1;697:24-28. doi: 10.1016/j.neulet.2018.05.033. Epub 2018 May 23.

DOI:10.1016/j.neulet.2018.05.033
PMID:29802916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6251759/
Abstract

As the sites of communication between neurons, synapses depend upon precisely regulated protein-protein interactions to support neurotransmitter release and reception. Moreover, neuronal synapses typically exist great distances (i.e. up to meters) away from cell bodies, which are the sources of new proteins and the major sites of protein degradation via lysosomes. Thus, synapses are uniquely sensitive to disruptions in proteostasis, and depend upon carefully orchestrated degradative mechanisms for the clearance of dysfunctional proteins. One of the primary cellular degradative pathways is macroautophagy, hereafter referred to as 'autophagy'. Although it has only recently become a focus of research in synaptic biology, emerging studies indicate that autophagy has essential functions at the synapse throughout an organism's lifetime. This review will discuss recent findings about the roles of synaptic autophagy, as well as some of the questions and issues to be considered in this field moving forward.

摘要

作为神经元之间的通讯位点,突触依赖于精确调控的蛋白质-蛋白质相互作用来支持神经递质的释放和接收。此外,神经元突触通常距离细胞体很远(即可达数米),而细胞体是新蛋白质的来源以及通过溶酶体进行蛋白质降解的主要位点。因此,突触对蛋白质稳态的破坏特别敏感,并依赖精心编排的降解机制来清除功能失调的蛋白质。细胞主要的降解途径之一是巨自噬,以下简称为“自噬”。尽管它直到最近才成为突触生物学研究的焦点,但新出现的研究表明,自噬在生物体的整个生命周期中对突触都具有重要功能。本综述将讨论关于突触自噬作用的最新发现,以及该领域未来需要考虑的一些问题。

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本文引用的文献

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Basal mitophagy is widespread in but minimally affected by loss of Pink1 or parkin.基础线粒体自噬在中广泛存在,但受 Pink1 或 parkin 缺失的影响最小。
J Cell Biol. 2018 May 7;217(5):1613-1622. doi: 10.1083/jcb.201801044. Epub 2018 Mar 2.
2
Autophagy in the presynaptic compartment in health and disease.健康与疾病状态下突触前区室的自噬
J Cell Biol. 2017 Jul 3;216(7):1895-1906. doi: 10.1083/jcb.201611113. Epub 2017 May 17.
3
PINK1/Parkin-Dependent Mitochondrial Surveillance: From Pleiotropy to Parkinson's Disease.PINK1/帕金蛋白依赖的线粒体监测:从多效性到帕金森病
神经元与神经胶质细胞之间以及神经胶质细胞与神经胶质细胞之间的信号传导指导关键期依赖经验的突触修剪。
Front Cell Dev Biol. 2025 Feb 18;13:1540052. doi: 10.3389/fcell.2025.1540052. eCollection 2025.
4
Inhibition of TrkB kinase activity impairs autophagy in cervical motor neurons of young but not old mice.抑制TrkB激酶活性会损害幼龄小鼠而非老龄小鼠颈髓运动神经元中的自噬。
Exp Physiol. 2025 Jan;110(1):166-178. doi: 10.1113/EP092095. Epub 2024 Nov 22.
5
Autophagy defects at weaning impair complement-dependent synaptic pruning and induce behavior deficits.断奶时自噬缺陷会损害补体依赖性突触修剪,并导致行为缺陷。
J Neuroinflammation. 2024 Sep 27;21(1):239. doi: 10.1186/s12974-024-03235-z.
6
Neurons Specialize in Presynaptic Autophagy: A Perspective to Ameliorate Neurodegeneration.神经元在突触前自噬方面具有特异性:改善神经退行性变的一个视角。
Mol Neurobiol. 2025 Feb;62(2):2626-2640. doi: 10.1007/s12035-024-04399-8. Epub 2024 Aug 14.
7
PTPRS is a novel marker for early Tau pathology and synaptic integrity in Alzheimer's disease.PTPRS 是阿尔茨海默病中早期 Tau 病理学和突触完整性的新型标志物。
Sci Rep. 2024 Jun 26;14(1):14718. doi: 10.1038/s41598-024-65104-2.
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Cell-specific alterations in autophagy-lysosomal activity near the chronically implanted microelectrodes.慢性植入的微电极附近自噬溶酶体活性的细胞特异性改变。
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Molecules. 2023 Feb 16;28(4):1889. doi: 10.3390/molecules28041889.
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Elife. 2023 Feb 2;12:e82568. doi: 10.7554/eLife.82568.
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