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Rab10失活在长时程增强过程中促进AMPA受体转运和树突棘增大。

Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation.

作者信息

Wang Jie, Nishiyama Jun, Parra-Bueno Paula, Okaz Elwy, Oz Goksu, Liu Xiaodan, Watabe Tetsuya, Suponitsky-Kroyter Irena, McGraw Timothy E, Szatmari Erzsebet M, Yasuda Ryohei

机构信息

Department of Neurobiology, Duke University School of Medicine, Durham, United States.

Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience, Jupiter, United States.

出版信息

Elife. 2025 Sep 23;13:RP103879. doi: 10.7554/eLife.103879.

DOI:10.7554/eLife.103879
PMID:40986440
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12456950/
Abstract

Rab-dependent membrane trafficking is critical for changing the structure and function of dendritic spines during synaptic plasticity. Here, we developed highly sensitive sensors to monitor Rab protein activity in single dendritic spines undergoing structural long-term potentiation (sLTP) in rodent organotypic hippocampal slices. During sLTP, Rab10 was persistently inactivated (>30 min) in the stimulated spines, whereas Rab4 was transiently activated over ~5 min. Inhibiting or deleting Rab10 enhanced sLTP, electrophysiological LTP, and AMPA receptor (AMPAR) trafficking during sLTP. In contrast, disrupting Rab4 impaired sLTP only in the first few minutes and decreased AMPAR trafficking during sLTP. Thus, our results suggest that Rab10 and Rab4 oppositely regulate AMPAR trafficking during sLTP, and inactivation of Rab10 signaling facilitates the induction of LTP and associated spine structural plasticity.

摘要

Rab 依赖性膜运输对于突触可塑性期间树突棘的结构和功能变化至关重要。在这里，我们开发了高度灵敏的传感器，以监测在啮齿动物海马脑片培养物中经历结构性长时程增强（sLTP）的单个树突棘中的 Rab 蛋白活性。在 sLTP 期间，Rab10 在受刺激的树突棘中持续失活（>30 分钟），而 Rab4 在约 5 分钟内短暂激活。抑制或缺失 Rab10 可增强 sLTP、电生理长时程增强（LTP）以及 sLTP 期间的 AMPA 受体（AMPAR）运输。相反，破坏 Rab4 仅在最初几分钟内损害 sLTP，并降低 sLTP 期间的 AMPAR 运输。因此，我们的结果表明，Rab10 和 Rab4 在 sLTP 期间对 AMPAR 运输起相反的调节作用，并且 Rab10 信号的失活促进了 LTP 的诱导以及相关的树突棘结构可塑性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/eed207cba46c/elife-103879-fig5-figsupp2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/c8d83bccb3f0/elife-103879-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/c89c40f68db0/elife-103879-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/42f4212b3a52/elife-103879-fig2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/c4d6d67e5c97/elife-103879-fig2-figsupp5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/0257180245d8/elife-103879-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/5a0d0edace99/elife-103879-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/968f1888b116/elife-103879-fig3-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/8e6a65ceb949/elife-103879-fig3-figsupp3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/ee01b7505433/elife-103879-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/0cd13926d455/elife-103879-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/7083666588e0/elife-103879-fig4-figsupp2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/3610f3c09108/elife-103879-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/431773fe6647/elife-103879-fig5-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c40/12456950/eed207cba46c/elife-103879-fig5-figsupp2.jpg

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本文引用的文献

1
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Nature. 2021 Dec;600(7890):686-689. doi: 10.1038/s41586-021-04125-7. Epub 2021 Nov 24.
2
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.
3
Rapid Ultrastructural Changes in the PSD and Surrounding Membrane after Induction of Structural LTP in Single Dendritic Spines.
快速结构型长时程增强诱导后 PSD 及其周围膜的超微结构变化
J Neurosci. 2021 Aug 18;41(33):7003-7014. doi: 10.1523/JNEUROSCI.1964-20.2021. Epub 2021 Jul 15.
4
RAB10: an Alzheimer's disease resilience locus and potential drug target.RAB10：阿尔茨海默病的抗性基因座和潜在的药物靶点。
Clin Interv Aging. 2018 Dec 28;14:73-79. doi: 10.2147/CIA.S159148. eCollection 2019.
5
Pre-post synaptic alignment through neuroligin-1 tunes synaptic transmission efficiency.通过神经黏附素-1实现突触前-后对准来调节突触传递效率。
Elife. 2018 Jul 25;7:e31755. doi: 10.7554/eLife.31755.
6
Linkage, whole genome sequence, and biological data implicate variants in RAB10 in Alzheimer's disease resilience.连锁分析、全基因组序列和生物学数据提示 RAB10 中的变异与阿尔茨海默病的抵抗能力有关。
Genome Med. 2017 Nov 29;9(1):100. doi: 10.1186/s13073-017-0486-1.
7
Coordination of AMPA receptor trafficking by Rab GTPases.Rab GTP 酶对 AMPA 受体转运的协调作用。
Small GTPases. 2019 Nov;10(6):419-432. doi: 10.1080/21541248.2017.1337546. Epub 2017 Jul 5.
8
CaMKII Autophosphorylation Is Necessary for Optimal Integration of Ca Signals during LTP Induction, but Not Maintenance.钙/钙调蛋白依赖性蛋白激酶II（CaMKII）自身磷酸化对于长时程增强（LTP）诱导过程中钙信号的最佳整合是必要的，但对于LTP维持并非必要。
Neuron. 2017 May 17;94(4):800-808.e4. doi: 10.1016/j.neuron.2017.04.041.
9
Postsynaptic synaptotagmins mediate AMPA receptor exocytosis during LTP.突触后突触结合蛋白在长时程增强过程中介导AMPA受体胞吐作用。
Nature. 2017 Apr 20;544(7650):316-321. doi: 10.1038/nature21720. Epub 2017 Mar 29.
10
Imaging ERK and PKA Activation in Single Dendritic Spines during Structural Plasticity.在结构可塑性过程中对单个树突棘中的细胞外信号调节激酶（ERK）和蛋白激酶A（PKA）激活进行成像
Neuron. 2017 Mar 22;93(6):1315-1324.e3. doi: 10.1016/j.neuron.2017.02.032. Epub 2017 Mar 9.