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光诱导小胶质细胞在成年大脑中聚焦重塑突触。

Light-induced engagement of microglia to focally remodel synapses in the adult brain.

机构信息

ESF International Graduate School on Analysis, Imaging and Modelling of Neuronal and Inflammatory Processes, Magdeburg, Germany.

Institut für Biochemie und Zellbiologie, Otto-von-Guericke-University, Medical Faculty, Magdeburg, Germany.

出版信息

Elife. 2020 Aug 18;9:e58435. doi: 10.7554/eLife.58435.

DOI:10.7554/eLife.58435
PMID:32808923
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7470825/
Abstract

Microglia continuously monitor synapses, but active synaptic remodeling by microglia in mature healthy brains is rarely directly observed. We performed targeted photoablation of single synapses in mature transgenic mice expressing fluorescent labels in neurons and microglia. The photodamage focally increased the duration of microglia-neuron contacts, and dramatically exacerbated both the turnover of dendritic spines and presynaptic boutons as well as the generation of new filopodia originating from spine heads or boutons. The results of microglia depletion confirmed that elevated spine turnover and the generation of presynaptic filopodia are microglia-dependent processes.

摘要

小胶质细胞持续监测突触,但在成熟健康大脑中,小胶质细胞的活跃突触重塑很少被直接观察到。我们在表达神经元和小胶质细胞荧光标记物的成熟转基因小鼠中,对单个突触进行了靶向光消融。光损伤使小胶质细胞-神经元接触的持续时间明显延长,并极大地加剧了树突棘和突触前末梢的周转,以及从棘突或末梢起始的新丝状伪足的产生。小胶质细胞耗竭的结果证实,升高的棘突周转和突触前丝状伪足的产生是依赖小胶质细胞的过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/16677e693cf6/elife-58435-fig3-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/4805528362b3/elife-58435-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/599ea7dfe8e3/elife-58435-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/5477423237f8/elife-58435-fig1-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/7a91e8cd8315/elife-58435-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/196c4df19445/elife-58435-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/59a1ce6f3c92/elife-58435-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/16677e693cf6/elife-58435-fig3-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/4805528362b3/elife-58435-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/599ea7dfe8e3/elife-58435-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/5477423237f8/elife-58435-fig1-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/7a91e8cd8315/elife-58435-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/196c4df19445/elife-58435-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/59a1ce6f3c92/elife-58435-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b9c/7470825/16677e693cf6/elife-58435-fig3-figsupp2.jpg

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Immune cell regulation of glia during CNS injury and disease.中枢神经系统损伤和疾病期间免疫细胞对神经胶质的调控。
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Microglia mediate forgetting via complement-dependent synaptic elimination.小胶质细胞通过补体依赖性突触消除来介导遗忘。
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