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巨噬细胞对于耳蜗带状突触的出生后修剪并非必需。

Macrophages Are Dispensable for Postnatal Pruning of the Cochlear Ribbon Synapses.

作者信息

Yu Chaorong, Gao Hui-Ming, Wan Guoqiang

机构信息

MOE Key Laboratory of Model Animal for Disease Study, Department of Otorhinolaryngology-Head and Neck Surgery, The Affiliated Drum Tower Hospital of Medical School, Model Animal Research Center of Medical School, Nanjing University, Nanjing, China.

Jiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, China.

出版信息

Front Cell Neurosci. 2021 Oct 21;15:736120. doi: 10.3389/fncel.2021.736120. eCollection 2021.

DOI:10.3389/fncel.2021.736120
PMID:34744631
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8566810/
Abstract

Ribbon synapses of cochlear hair cells undergo pruning and maturation before the hearing onset. In the central nervous system (CNS), synaptic pruning was mediated by microglia, the brain-resident macrophages, activation of the complement system. Whether a similar mechanism regulates ribbon synapse pruning is currently unknown. In this study, we report that the densities of cochlear macrophages surrounding hair cells were highest at around P8, corresponding well to the completion of ribbon synaptic pruning by P8-P9. Surprisingly, using multiple genetic mouse models, we found that postnatal pruning of the ribbon synapses and auditory functions were unaffected by the knockout of the complement receptor 3 (CR3) or by ablations of macrophages expressing either LysM or Cx3cr1. Our results suggest that unlike microglia in the CNS, macrophages in the cochlea do not mediate pruning of the cochlear ribbon synapses.

摘要

耳蜗毛细胞的带状突触在听力开始前会经历修剪和成熟过程。在中枢神经系统(CNS)中,突触修剪是由小胶质细胞(即驻留在大脑中的巨噬细胞)介导的,通过补体系统的激活来实现。目前尚不清楚是否有类似机制调节带状突触的修剪。在本研究中,我们报告称,围绕毛细胞的耳蜗巨噬细胞密度在出生后第8天左右最高,这与出生后第8至9天带状突触修剪的完成情况高度吻合。令人惊讶的是,使用多种基因小鼠模型,我们发现带状突触的出生后修剪和听觉功能不受补体受体3(CR3)敲除或表达LysM或Cx3cr1的巨噬细胞消融的影响。我们的结果表明,与中枢神经系统中的小胶质细胞不同,耳蜗中的巨噬细胞不介导耳蜗带状突触的修剪。

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引用本文的文献

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Cochlear resident macrophage mediates development of ribbon synapses CX3CR1/CX3CL1 axis.耳蜗驻留巨噬细胞通过CX3CR1/CX3CL1轴介导带状突触的发育。
Front Mol Neurosci. 2022 Nov 28;15:1031278. doi: 10.3389/fnmol.2022.1031278. eCollection 2022.

本文引用的文献

1
Deletion of Causes Hearing Loss and Abnormal Auditory Nerve Fibers in the Mouse Cochlea.基因缺失导致小鼠耳蜗听力丧失及听觉神经纤维异常。
Front Cell Neurosci. 2021 Aug 25;15:713651. doi: 10.3389/fncel.2021.713651. eCollection 2021.
2
The immune response after noise damage in the cochlea is characterized by a heterogeneous mix of adaptive and innate immune cells.耳蜗噪声损伤后的免疫反应以适应性和固有免疫细胞的异质混合为特征。
Sci Rep. 2020 Sep 16;10(1):15167. doi: 10.1038/s41598-020-72181-6.
3
Early Development of Resident Macrophages in the Mouse Cochlea Depends on Yolk Sac Hematopoiesis.
小鼠耳蜗中驻留巨噬细胞的早期发育依赖于卵黄囊造血作用。
Front Neurol. 2019 Oct 22;10:1115. doi: 10.3389/fneur.2019.01115. eCollection 2019.
4
Lack of Fractalkine Receptor on Macrophages Impairs Spontaneous Recovery of Ribbon Synapses After Moderate Noise Trauma in C57BL/6 Mice.巨噬细胞上缺乏趋化因子受体损害C57BL/6小鼠中度噪声损伤后带状突触的自发恢复。
Front Neurosci. 2019 Jun 13;13:620. doi: 10.3389/fnins.2019.00620. eCollection 2019.
5
Mapping developmental maturation of inner hair cell ribbon synapses in the apical mouse cochlea.绘制顶端小鼠耳蜗内毛细胞带状突触发育成熟图谱。
Proc Natl Acad Sci U S A. 2019 Mar 26;116(13):6415-6424. doi: 10.1073/pnas.1812029116. Epub 2019 Mar 13.
6
Current concepts in cochlear ribbon synapse formation.当前耳蜗带状突触形成的概念。
Synapse. 2019 May;73(5):e22087. doi: 10.1002/syn.22087. Epub 2019 Feb 18.
7
Interactions between Macrophages and the Sensory Cells of the Inner Ear.巨噬细胞与内耳感觉细胞的相互作用。
Cold Spring Harb Perspect Med. 2019 Jun 3;9(6):a033555. doi: 10.1101/cshperspect.a033555.
8
Differential fates of tissue macrophages in the cochlea during postnatal development.出生后发育过程中耳蜗组织巨噬细胞的命运差异。
Hear Res. 2018 Aug;365:110-126. doi: 10.1016/j.heares.2018.05.010. Epub 2018 May 16.
9
Macrophage-Mediated Glial Cell Elimination in the Postnatal Mouse Cochlea.出生后小鼠耳蜗中巨噬细胞介导的神经胶质细胞清除
Front Mol Neurosci. 2017 Dec 11;10:407. doi: 10.3389/fnmol.2017.00407. eCollection 2017.
10
Genetic disruption of fractalkine signaling leads to enhanced loss of cochlear afferents following ototoxic or acoustic injury.趋化因子信号的基因破坏导致耳毒性或声学损伤后耳蜗传入神经的损失增加。
J Comp Neurol. 2018 Apr 1;526(5):824-835. doi: 10.1002/cne.24369. Epub 2017 Dec 17.