• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

突触活动通过不同的再循环途径调节AMPA受体的转运。

Synaptic activity regulates AMPA receptor trafficking through different recycling pathways.

作者信息

Zheng Ning, Jeyifous Okunola, Munro Charlotte, Montgomery Johanna M, Green William N

机构信息

Department of Neurobiology, University of Chicago, Chicago, United States.

Department of Physiology, University of Auckland, Auckland, New Zealand.

出版信息

Elife. 2015 May 13;4:e06878. doi: 10.7554/eLife.06878.

DOI:10.7554/eLife.06878
PMID:25970033
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4451724/
Abstract

Changes in glutamatergic synaptic strength in brain are dependent on AMPA-type glutamate receptor (AMPAR) recycling, which is assumed to occur through a single local pathway. In this study, we present evidence that AMPAR recycling occurs through different pathways regulated by synaptic activity. Without synaptic stimulation, most AMPARs recycled in dynamin-independent endosomes containing the GTPase, Arf6. Few AMPARs recycled in dynamin-dependent endosomes labeled by transferrin receptors (TfRs). AMPAR recycling was blocked by alterations in the GTPase, TC10, which co-localized with Arf6 endosomes. TC10 mutants that reduced AMPAR recycling had no effect on increased AMPAR levels with long-term potentiation (LTP) and little effect on decreased AMPAR levels with long-term depression. However, internalized AMPAR levels in TfR-containing recycling endosomes increased after LTP, indicating increased AMPAR recycling through the dynamin-dependent pathway with synaptic plasticity. LTP-induced AMPAR endocytosis is inconsistent with local recycling as a source of increased surface receptors, suggesting AMPARs are trafficked from other sites.

摘要

大脑中谷氨酸能突触强度的变化取决于AMPA型谷氨酸受体（AMPAR）的循环利用，一般认为其通过单一局部途径发生。在本研究中，我们提供证据表明AMPAR循环利用通过受突触活动调节的不同途径发生。在没有突触刺激的情况下，大多数AMPAR在含有GTP酶Arf6的发动蛋白非依赖性内体中循环利用。少数AMPAR在由转铁蛋白受体（TfRs）标记的发动蛋白依赖性内体中循环利用。AMPAR循环利用被与Arf6内体共定位的GTP酶TC10的改变所阻断。降低AMPAR循环利用的TC10突变体对长期增强（LTP）导致的AMPAR水平升高没有影响，对长期抑制导致的AMPAR水平降低影响也很小。然而，LTP后含TfR的循环内体中内化的AMPAR水平增加，表明随着突触可塑性，通过发动蛋白依赖性途径的AMPAR循环利用增加。LTP诱导的AMPAR内吞作用与作为表面受体增加来源的局部循环利用不一致，这表明AMPAR是从其他部位转运而来的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/27a30b61afa0/elife06878f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/4f39bd862a63/elife06878f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/ff7ea4e5d9e4/elife06878fs001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/880e7b705218/elife06878fs002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/4b03f133d27b/elife06878fs003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/94fe38b5d19d/elife06878fs004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/ee7ca6a73f29/elife06878fs005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/b19696197966/elife06878fs006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/62a93ffc9e24/elife06878f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/e67c17e54b3b/elife06878fs007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/3b3185bc0eb3/elife06878f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/728612c37f07/elife06878f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/b203fff24bf7/elife06878fs008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/9542a1b99449/elife06878f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/27a30b61afa0/elife06878f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/4f39bd862a63/elife06878f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/ff7ea4e5d9e4/elife06878fs001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/880e7b705218/elife06878fs002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/4b03f133d27b/elife06878fs003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/94fe38b5d19d/elife06878fs004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/ee7ca6a73f29/elife06878fs005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/b19696197966/elife06878fs006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/62a93ffc9e24/elife06878f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/e67c17e54b3b/elife06878fs007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/3b3185bc0eb3/elife06878f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/728612c37f07/elife06878f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/b203fff24bf7/elife06878fs008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/9542a1b99449/elife06878f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5a/4451724/27a30b61afa0/elife06878f006.jpg

相似文献

1
Synaptic activity regulates AMPA receptor trafficking through different recycling pathways.突触活动通过不同的再循环途径调节AMPA受体的转运。
Elife. 2015 May 13;4:e06878. doi: 10.7554/eLife.06878.
2
Recycling endosomes supply AMPA receptors for LTP.再循环内体为长时程增强提供AMPA受体。
Science. 2004 Sep 24;305(5692):1972-5. doi: 10.1126/science.1102026.
3
Postsynaptic density 95 controls AMPA receptor incorporation during long-term potentiation and experience-driven synaptic plasticity.突触后致密蛋白95在长时程增强和经验驱动的突触可塑性过程中控制AMPA受体的整合。
J Neurosci. 2004 Jan 28;24(4):916-27. doi: 10.1523/JNEUROSCI.4733-03.2004.
4
BRAG2a Mediates mGluR-Dependent AMPA Receptor Internalization at Excitatory Postsynapses through the Interaction with PSD-95 and Endophilin 3.BRAG2a 通过与 PSD-95 和内收蛋白 3 的相互作用介导谷氨酸能突触后 AMPA 受体的 mGluR 依赖性内化。
J Neurosci. 2020 May 27;40(22):4277-4296. doi: 10.1523/JNEUROSCI.1645-19.2020. Epub 2020 Apr 27.
5
Subunit-dependent and subunit-independent rules of AMPA receptor trafficking during chemical long-term depression in hippocampal neurons.AMPA 受体在海马神经元化学长时程压抑过程中的亚基依赖性和非亚基依赖性转运规律。
J Biol Chem. 2021 Aug;297(2):100949. doi: 10.1016/j.jbc.2021.100949. Epub 2021 Jul 10.
6
Endosomal sorting of AMPA receptors in hippocampal neurons.在海马神经元中 AMPA 受体的内体分拣。
Biochem Soc Trans. 2010 Apr;38(2):460-5. doi: 10.1042/BST0380460.
7
Role of AMPA receptor trafficking in NMDA receptor-dependent synaptic plasticity in the rat lateral amygdala.AMPA受体转运在大鼠外侧杏仁核NMDA受体依赖性突触可塑性中的作用
J Neurochem. 2008 Jul;106(2):889-99. doi: 10.1111/j.1471-4159.2008.05461.x. Epub 2008 May 4.
8
A retention-release mechanism based on RAB11FIP2 for AMPA receptor synaptic delivery during long-term potentiation.基于 RAB11FIP2 的内吞释放机制促进长时程增强过程中 AMPA 受体的突触传递。
J Cell Sci. 2019 Dec 16;132(24):jcs234237. doi: 10.1242/jcs.234237.
9
Endosomal trafficking of AMPA-type glutamate receptors.AMPA 型谷氨酸受体的内体运输
Neuroscience. 2009 Jan 12;158(1):36-44. doi: 10.1016/j.neuroscience.2008.02.057. Epub 2008 Mar 6.
10
Palmitoylation of A-kinase anchoring protein 79/150 regulates dendritic endosomal targeting and synaptic plasticity mechanisms.棕榈酰化 A-激酶锚定蛋白 79/150 调节树突内体靶向和突触可塑性机制。
J Neurosci. 2012 May 23;32(21):7119-36. doi: 10.1523/JNEUROSCI.0784-12.2012.

引用本文的文献

1
Long-term potentiation-induced changes in actin dynamics and spine geometry persist on the timescale of the synaptic tag.长时程增强诱导的肌动蛋白动力学和棘突几何形状的变化在突触标记的时间尺度上持续存在。
Commun Biol. 2025 Jul 18;8(1):1065. doi: 10.1038/s42003-025-08459-0.
2
Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling.SynDIG4/PRRT1的缺失改变了AMPA受体在Rab4和Rab11阳性内体中的分布，并损害了基础AMPA受体的再循环。
Front Pharmacol. 2025 May 21;16:1568908. doi: 10.3389/fphar.2025.1568908. eCollection 2025.
3
Loss of the proton-activated chloride channel in neurons impairs AMPA receptor endocytosis and LTD via endosomal hyper-acidification.

本文引用的文献

1
GTP hydrolysis of TC10 promotes neurite outgrowth through exocytic fusion of Rab11- and L1-containing vesicles by releasing exocyst component Exo70.TC10的GTP水解通过释放外排体成分Exo70，促进含Rab11和L1的囊泡的胞吐融合，从而促进神经突生长。
PLoS One. 2013 Nov 4;8(11):e79689. doi: 10.1371/journal.pone.0079689. eCollection 2013.
2
The balance between receptor recycling and trafficking toward lysosomes determines synaptic strength during long-term depression.在长时程压抑过程中，受体的再循环和向溶酶体运输之间的平衡决定了突触强度。
J Neurosci. 2012 Sep 19;32(38):13200-5. doi: 10.1523/JNEUROSCI.0061-12.2012.
3
Harnessing the power of the endosome to regulate neural development.
神经元中质子激活氯离子通道的缺失通过内体过度酸化损害AMPA受体内吞作用和长时程抑制。
Cell Rep. 2025 Feb 25;44(2):115302. doi: 10.1016/j.celrep.2025.115302. Epub 2025 Feb 12.
4
Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling.SynDIG4/PRRT1的缺失改变了AMPA受体在Rab4和Rab11阳性内体中的分布，并损害了基础AMPA受体循环。
bioRxiv. 2024 Dec 29:2024.12.29.630674. doi: 10.1101/2024.12.29.630674.
5
The Role of Extracellular Vesicles and Microparticles in Central Nervous System Disorders: Mechanisms, Biomarkers, and Therapeutic Potential.细胞外囊泡和微粒在中枢神经系统疾病中的作用：机制、生物标志物及治疗潜力
Cell Mol Neurobiol. 2024 Dec 3;44(1):82. doi: 10.1007/s10571-024-01518-w.
6
G272V and P301L Mutations Induce Isoform Specific Tau Mislocalization to Dendritic Spines and Synaptic Dysfunctions in Cellular Models of 3R and 4R Tau Frontotemporal Dementia.G272V 和 P301L 突变导致 3R 和 4R tau 额颞叶痴呆细胞模型中异构体特异性 tau 向树突棘的异常定位和突触功能障碍。
J Neurosci. 2024 Jul 10;44(28):e1215232024. doi: 10.1523/JNEUROSCI.1215-23.2024.
7
Muscarinic acetylcholine receptor-dependent and NMDA receptor-dependent LTP and LTD share the common AMPAR trafficking pathway.毒蕈碱型乙酰胆碱受体依赖性和NMDA受体依赖性长时程增强和长时程抑制共享共同的AMPA受体转运途径。
iScience. 2023 Feb 3;26(3):106133. doi: 10.1016/j.isci.2023.106133. eCollection 2023 Mar 17.
8
The Role of Zinc and NMDA Receptors in Autism Spectrum Disorders.锌与N-甲基-D-天冬氨酸受体在自闭症谱系障碍中的作用
Pharmaceuticals (Basel). 2022 Dec 20;16(1):1. doi: 10.3390/ph16010001.
9
Rho Signaling in Synaptic Plasticity, Memory, and Brain Disorders.Rho信号传导在突触可塑性、记忆及脑部疾病中的作用
Front Cell Dev Biol. 2021 Oct 4;9:729076. doi: 10.3389/fcell.2021.729076. eCollection 2021.
10
Auxiliary Subunits Regulate the Dendritic Turnover of AMPA Receptors in Mouse Hippocampal Neurons.辅助亚基调节小鼠海马神经元中AMPA受体的树突周转
Front Mol Neurosci. 2021 Aug 23;14:728498. doi: 10.3389/fnmol.2021.728498. eCollection 2021.
利用内体的力量来调节神经发育。
Neuron. 2012 May 10;74(3):440-51. doi: 10.1016/j.neuron.2012.04.015.
4
Postsynaptic complexin controls AMPA receptor exocytosis during LTP.突触后复合蛋白在 LTP 期间控制 AMPA 受体胞吐。
Neuron. 2012 Jan 26;73(2):260-7. doi: 10.1016/j.neuron.2011.11.020.
5
Distinct recycling of active and inactive β1 integrins.β1 整联蛋白的活性和非活性亚基的特异性回收。
Traffic. 2012 Apr;13(4):610-25. doi: 10.1111/j.1600-0854.2012.01327.x. Epub 2012 Jan 31.
6
Regulation of AMPA receptor surface diffusion by PSD-95 slots.PSD-95 槽调控 AMPA 受体表面扩散。
Curr Opin Neurobiol. 2012 Jun;22(3):453-60. doi: 10.1016/j.conb.2011.10.010. Epub 2011 Nov 1.
7
Regional and subcellular distribution of the receptor-targeting protein PIST in the rat central nervous system.大鼠中枢神经系统中受体靶向蛋白 PIST 的区域和亚细胞分布。
J Comp Neurol. 2012 Apr 1;520(5):889-913. doi: 10.1002/cne.22774.
8
SAP97 directs NMDA receptor spine targeting and synaptic plasticity.SAP97 指导 NMDA 受体棘突定位和突触可塑性。
J Physiol. 2011 Sep 15;589(Pt 18):4491-510. doi: 10.1113/jphysiol.2011.215566. Epub 2011 Jul 18.
9
Trafficking of AMPA receptors at plasma membranes of hippocampal neurons.AMPA 受体在海马神经元质膜中的转运。
J Neurosci. 2011 Mar 30;31(13):4834-43. doi: 10.1523/JNEUROSCI.4745-10.2011.
10
Role of syntaxin 4 in activity-dependent exocytosis and synaptic plasticity in hippocampal neurons.突触融合蛋白 4 在海马神经元活动依赖性胞吐作用和突触可塑性中的作用。
Sci Signal. 2010 Oct 19;3(144):jc7. doi: 10.1126/scisignal.3144jc7.