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本文引用的文献

1
miR-124-dependent tagging of synapses by synaptopodin enables input-specific homeostatic plasticity.miR-124 通过突触足蛋白对突触的标记作用实现了输入特异性的平衡型可塑性。
EMBO J. 2022 Oct 17;41(20):e109012. doi: 10.15252/embj.2021109012. Epub 2022 Jul 25.
2
Pervasive compartment-specific regulation of gene expression during homeostatic synaptic scaling.在稳态突触缩放过程中,基因表达的普遍隔室特异性调节。
EMBO Rep. 2021 Oct 5;22(10):e52094. doi: 10.15252/embr.202052094. Epub 2021 Aug 16.
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Illuminating dendritic function with computational models.用计算模型照亮树突功能。
Nat Rev Neurosci. 2020 Jun;21(6):303-321. doi: 10.1038/s41583-020-0301-7. Epub 2020 May 11.
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Primed to Sleep: The Dynamics of Synaptic Plasticity Across Brain States.准备入睡:跨脑状态的突触可塑性动态变化
Front Syst Neurosci. 2019 Feb 1;13:2. doi: 10.3389/fnsys.2019.00002. eCollection 2019.
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Homer1a drives homeostatic scaling-down of excitatory synapses during sleep.荷马1a在睡眠期间驱动兴奋性突触的稳态缩小。
Science. 2017 Feb 3;355(6324):511-515. doi: 10.1126/science.aai8355. Epub 2017 Feb 2.
6
Sleep and the price of plasticity: from synaptic and cellular homeostasis to memory consolidation and integration.睡眠与可塑性的代价:从突触和细胞的稳态到记忆的巩固和整合。
Neuron. 2014 Jan 8;81(1):12-34. doi: 10.1016/j.neuron.2013.12.025.
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Synaptopodin regulates denervation-induced homeostatic synaptic plasticity.突触足蛋白调节去神经诱导的代偿性突触可塑性。
Proc Natl Acad Sci U S A. 2013 May 14;110(20):8242-7. doi: 10.1073/pnas.1213677110. Epub 2013 Apr 29.
8
microRNAs at the synapse.突触处的微小RNA
Nat Rev Neurosci. 2009 Dec;10(12):842-9. doi: 10.1038/nrn2763. Epub 2009 Nov 4.
9
The self-tuning neuron: synaptic scaling of excitatory synapses.自调节神经元:兴奋性突触的突触缩放
Cell. 2008 Oct 31;135(3):422-35. doi: 10.1016/j.cell.2008.10.008.
10
Two opposing plasticity mechanisms pulling a single synapse.两种相反的可塑性机制作用于单个突触。
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突触标记:动态平衡的可塑性遵循赫布法则。

Synaptic tagging: homeostatic plasticity goes Hebbian.

机构信息

Laboratory of Systems Neuroscience, Institute for Neuroscience, Department of Health Science and Technology, Swiss Federal Institute of Technology ETH, Zürich, Switzerland.

出版信息

EMBO J. 2022 Oct 17;41(20):e112383. doi: 10.15252/embj.2022112383. Epub 2022 Sep 13.

DOI:10.15252/embj.2022112383
PMID:36097740
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9574739/
Abstract

Distinct plasticity mechanisms enable neurons to effectively process information also when facing global perturbations in network activity. In this issue of The EMBO Journal, Dubes et al (2022) provide a molecular mechanism whereby individual synapses during periods of chronic inactivity are "tagged" for future strengthening. These results lend further support to the idea that local, nonmultiplicative mechanisms play an important role in homeostatic synaptic plasticity as has been demonstrated for Hebbian-like synaptic plasticity.

摘要

当面临网络活动的全局干扰时,不同的可塑性机制使神经元能够有效地处理信息。在本期《欧洲分子生物学组织杂志》中,Dubes 等人提供了一种分子机制,通过该机制,在慢性失活期间,个别突触会被“标记”以备将来增强。这些结果进一步支持了这样一种观点,即局部的、非倍增的机制在稳态突触可塑性中发挥着重要作用,正如在类赫布突触可塑性中所证明的那样。