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双光子显微镜下树突棘结构可塑性的成像。

Imaging of Structural Plasticity of Dendritic Spines with Two-Photon Microscopy.

机构信息

Department of Life Science and Technology, School of Life Science and Technology, Tokyo Institute of Technology, Kanagawa, Japan.

Department of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.

出版信息

Methods Mol Biol. 2024;2831:209-217. doi: 10.1007/978-1-0716-3969-6_14.

DOI:10.1007/978-1-0716-3969-6_14
PMID:39134852
Abstract

Plasticity of synaptic transmission underlies learning and memory. It is accompanied by changes in the density and size of synapses, collectively called structural plasticity. Therefore, understanding the mechanism of structural plasticity is critical for understanding the mechanism of synaptic plasticity. In this chapter, we describe the procedures and equipment required to image structural plasticity of a single dendritic spine, which hosts excitatory synapses in the central nervous system, and underlying molecular interactions/biochemical reactions using two-photon fluorescence lifetime microscopy (2P-FLIM) in combination with Förster resonance energy transfer (FRET)-based biosensors.

摘要

突触传递的可塑性是学习和记忆的基础。它伴随着突触密度和大小的变化,统称为结构可塑性。因此,了解结构可塑性的机制对于理解突触可塑性的机制至关重要。在本章中,我们描述了使用双光子荧光寿命显微镜(2P-FLIM)结合基于Förster 共振能量转移(FRET)的生物传感器来成像中枢神经系统中兴奋性突触所在的单个树突棘的结构可塑性,以及潜在的分子相互作用/生化反应所需的程序和设备。

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Imaging of Structural Plasticity of Dendritic Spines with Two-Photon Microscopy.双光子显微镜下树突棘结构可塑性的成像。
Methods Mol Biol. 2024;2831:209-217. doi: 10.1007/978-1-0716-3969-6_14.
2
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本文引用的文献

1
Stepwise synaptic plasticity events drive the early phase of memory consolidation.逐步的突触可塑性事件驱动记忆巩固的早期阶段。
Science. 2021 Nov 12;374(6569):857-863. doi: 10.1126/science.abj9195. Epub 2021 Nov 11.
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Reciprocal activation within a kinase effector complex: A mechanism for the persistence of molecular memory.激酶效应物复合物内的相互激活:分子记忆持续存在的一种机制。
Brain Res Bull. 2021 May;170:58-64. doi: 10.1016/j.brainresbull.2021.01.018. Epub 2021 Feb 5.
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Reciprocal Activation within a Kinase-Effector Complex Underlying Persistence of Structural LTP.
激酶-效应物复合物内的相互激活是结构型长时程增强持续存在的基础。
Neuron. 2019 Jun 19;102(6):1199-1210.e6. doi: 10.1016/j.neuron.2019.04.012. Epub 2019 May 8.
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Long-Term Potentiation: From CaMKII to AMPA Receptor Trafficking.长时程增强:从钙/钙调蛋白依赖性蛋白激酶II到α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体转运
Annu Rev Physiol. 2016;78:351-65. doi: 10.1146/annurev-physiol-021014-071753.
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Structural and molecular remodeling of dendritic spine substructures during long-term potentiation.长期增强过程中树突棘亚结构的结构和分子重塑。
Neuron. 2014 Apr 16;82(2):444-59. doi: 10.1016/j.neuron.2014.03.021.
6
Long-term depression triggers the selective elimination of weakly integrated synapses.长期抑郁会引发弱整合突触的选择性消除。
Proc Natl Acad Sci U S A. 2013 Nov 19;110(47):E4510-9. doi: 10.1073/pnas.1315926110. Epub 2013 Nov 4.
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Application of FRET probes in the analysis of neuronal plasticity.荧光共振能量转移探针在神经元可塑性分析中的应用。
Front Neural Circuits. 2013 Oct 10;7:163. doi: 10.3389/fncir.2013.00163. eCollection 2013.
8
Synapse-specific and size-dependent mechanisms of spine structural plasticity accompanying synaptic weakening.伴随突触弱化的突触特异性和尺寸依赖性的脊柱结构可塑性机制。
Proc Natl Acad Sci U S A. 2013 Jan 22;110(4):E305-12. doi: 10.1073/pnas.1214705110. Epub 2012 Dec 26.
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The Ca2+ and Rho GTPase signaling pathways underlying activity-dependent actin remodeling at dendritic spines.活性依赖的树突棘处肌动蛋白重塑的钙离子和 Rho GTPase 信号通路。
Cytoskeleton (Hoboken). 2012 Aug;69(8):545-54. doi: 10.1002/cm.21037. Epub 2012 May 22.
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Structural plasticity of dendritic spines.树突棘的结构可塑性。
Curr Opin Neurobiol. 2012 Jun;22(3):383-8. doi: 10.1016/j.conb.2011.09.002. Epub 2011 Sep 28.