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神经胶质细胞在突触发育中的作用。

Roles of glial cells in synapse development.

作者信息

Pfrieger Frank W

机构信息

Institute of Cellular and Integrative Neurosciences, CNRS UPR-3212, University of Strasbourg, 5, rue Louis Pasteur, 67084, Strasbourg, France.

出版信息

Cell Mol Life Sci. 2009 Jul;66(13):2037-47. doi: 10.1007/s00018-009-0005-7. Epub 2009 Mar 24.

DOI:10.1007/s00018-009-0005-7
PMID:19308323
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2705714/
Abstract

Brain function relies on communication among neurons via highly specialized contacts, the synapses, and synaptic dysfunction lies at the heart of age-, disease-, and injury-induced defects of the nervous system. For these reasons, the formation-and repair-of synaptic connections is a major focus of neuroscience research. In this review, I summarize recent evidence that synapse development is not a cell-autonomous process and that its distinct phases depend on assistance from the so-called glial cells. The results supporting this view concern synapses in the central nervous system as well as neuromuscular junctions and originate from experimental models ranging from cell cultures to living flies, worms, and mice. Peeking at the future, I will highlight recent technical advances that are likely to revolutionize our views on synapse-glia interactions in the developing, adult and diseased brain.

摘要

脑功能依赖于神经元之间通过高度特化的接触点——突触进行的通讯,而突触功能障碍是衰老、疾病和损伤所致神经系统缺陷的核心所在。基于这些原因,突触连接的形成与修复是神经科学研究的一个主要焦点。在这篇综述中,我总结了近期的证据,即突触发育并非一个细胞自主的过程,其不同阶段依赖于所谓神经胶质细胞的协助。支持这一观点的结果涉及中枢神经系统以及神经肌肉接头处的突触,且源自从细胞培养到活体果蝇、蠕虫和小鼠等多种实验模型。展望未来,我将重点介绍近期的技术进展,这些进展可能会彻底改变我们对发育中的、成年的和患病大脑中突触-神经胶质细胞相互作用的看法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/11115893/1cb44dbbdf55/18_2009_5_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/11115893/b82c7788778c/18_2009_5_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/11115893/1cb44dbbdf55/18_2009_5_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/11115893/b82c7788778c/18_2009_5_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/11115893/1cb44dbbdf55/18_2009_5_Fig2_HTML.jpg

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2
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3
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Mol Psychiatry. 2025 Mar;30(3):1019-1028. doi: 10.1038/s41380-024-02740-0. Epub 2024 Sep 5.
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