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用于研究中枢神经系统中活动依赖性髓鞘形成的新型工具箱。

Novel Toolboxes for the Investigation of Activity-Dependent Myelination in the Central Nervous System.

作者信息

Heflin Jack Kent, Sun Wenjing

机构信息

Department of Neuroscience, Wexner Medical Center, The Ohio State University, Columbus, OH, United States.

出版信息

Front Cell Neurosci. 2021 Nov 2;15:769809. doi: 10.3389/fncel.2021.769809. eCollection 2021.

DOI:10.3389/fncel.2021.769809
PMID:34795563
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8592894/
Abstract

Myelination is essential for signal processing within neural networks. Emerging data suggest that neuronal activity positively instructs myelin development and myelin adaptation during adulthood. However, the underlying mechanisms controlling activity-dependent myelination have not been fully elucidated. Myelination is a multi-step process that involves the proliferation and differentiation of oligodendrocyte precursor cells followed by the initial contact and ensheathment of axons by mature oligodendrocytes. Conventional end-point studies rarely capture the dynamic interaction between neurons and oligodendrocyte lineage cells spanning such a long temporal window. Given that such interactions and downstream signaling cascades are likely to occur within fine cellular processes of oligodendrocytes and their precursor cells, overcoming spatial resolution limitations represents another technical hurdle in the field. In this mini-review, we discuss how advanced genetic, cutting-edge imaging, and electrophysiological approaches enable us to investigate neuron-oligodendrocyte lineage cell interaction and myelination with both temporal and spatial precision.

摘要

髓鞘形成对于神经网络中的信号处理至关重要。新出现的数据表明,神经元活动在成年期对髓鞘发育和髓鞘适应性具有正向指导作用。然而,控制活动依赖性髓鞘形成的潜在机制尚未完全阐明。髓鞘形成是一个多步骤过程,涉及少突胶质细胞前体细胞的增殖和分化,随后是成熟少突胶质细胞与轴突的初始接触和包裹。传统的终点研究很少能捕捉到跨越如此长的时间窗口的神经元与少突胶质细胞谱系细胞之间的动态相互作用。鉴于这种相互作用和下游信号级联反应可能发生在少突胶质细胞及其前体细胞的精细细胞过程中,克服空间分辨率限制是该领域的另一个技术障碍。在本综述中,我们讨论了先进的遗传学、前沿成像和电生理学方法如何使我们能够以时间和空间精度研究神经元-少突胶质细胞谱系细胞相互作用和髓鞘形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/152d/8592894/3875b3bbd200/fncel-15-769809-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/152d/8592894/6a7757d794bf/fncel-15-769809-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/152d/8592894/3875b3bbd200/fncel-15-769809-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/152d/8592894/6a7757d794bf/fncel-15-769809-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/152d/8592894/3875b3bbd200/fncel-15-769809-g002.jpg

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本文引用的文献

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Myelination induces axonal hotspots of synaptic vesicle fusion that promote sheath growth.髓鞘化诱导轴突突触囊泡融合的热点,从而促进鞘的生长。
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Enhancing myelin renewal reverses cognitive dysfunction in a murine model of Alzheimer's disease.增强髓鞘更新可逆转阿尔茨海默病小鼠模型的认知功能障碍。
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GluA2 overexpression in oligodendrocyte progenitors promotes postinjury oligodendrocyte regeneration.
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Myelination of parvalbumin interneurons shapes the function of cortical sensory inhibitory circuits.少突胶质细胞髓鞘形成 parvalbumin 中间神经元塑造皮质感觉抑制回路的功能。
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Motor learning promotes remyelination via new and surviving oligodendrocytes.运动学习通过新的和存活的少突胶质细胞促进髓鞘再生。
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Functionally distinct subgroups of oligodendrocyte precursor cells integrate neural activity and execute myelin formation.功能不同的少突胶质前体细胞亚群整合神经活动并执行髓鞘形成。
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Preservation of a remote fear memory requires new myelin formation.远程恐惧记忆的保存需要新的髓鞘形成。
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Reduction of AMPA receptor activity on mature oligodendrocytes attenuates loss of myelinated axons in autoimmune neuroinflammation.降低成熟少突胶质细胞上 AMPA 受体的活性可减轻自身免疫性神经炎症中髓鞘轴突的丢失。
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