• 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

树突棘在成年大脑中的 Rho GTPase 依赖性可塑性。

Rho GTPase-dependent plasticity of dendritic spines in the adult brain.

机构信息

Department of Therapeutic Research and Medicines Evaluation, Istituto Superiore di Sanità Roma, Italy.

出版信息

Front Cell Neurosci. 2013 May 23;7:62. doi: 10.3389/fncel.2013.00062. eCollection 2013.

DOI:10.3389/fncel.2013.00062
PMID:23734098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3661998/
Abstract

Brain activity is associated with structural changes in the neural connections. However, in vivo imaging of the outer cortical layers has shown that dendritic spines, on which most excitatory synapses insist, are predominantly stable in adulthood. Changes in dendritic spines are governed by small GTPases of the Rho family through modulation of the actin cytoskeleton. Yet, while there are abundant data about this functional effect of Rho GTPases in vitro, there is limited evidence that Rho GTPase signaling in the brain is associated with changes in neuronal morphology. In the present work, both chronic in vivo two-photon imaging and Golgi staining reveal that the activation of Rho GTPases in the adult mouse brain is associated with little change of dendritic spines in the apical dendrites of primary visual cortex pyramidal neurons. On the contrary, considerable increase in spine density is observed (i) in the basal dendrites of the same neurons (ii) in both basal and apical dendrites of the hippocampal CA1 pyramidal cells. While confirming that Rho GTPase-dependent increase in spine density can be substantial, the study indicates region and dendrite selectivity with relative stability of superficial cortical circuits.

摘要

大脑活动与神经连接的结构变化有关。然而,对皮质外层层的活体成像显示,树突棘(其上附着大多数兴奋性突触)在成年期主要是稳定的。树突棘的变化受 Rho 家族的小 GTP 酶通过调节肌动蛋白细胞骨架来控制。然而,尽管有大量关于 Rho GTPase 在体外的这种功能效应的数据,但有限的证据表明大脑中的 Rho GTPase 信号与神经元形态的变化有关。在本工作中,慢性活体双光子成像和高尔基染色均显示,成年小鼠大脑中 Rho GTPase 的激活与初级视觉皮层锥体神经元顶树突棘的微小变化有关。相反,在同一神经元的基底树突(ii)和海马 CA1 锥体神经元的基底和顶树突中均观察到棘密度的显著增加(ii)。该研究既证实了 Rho GTPase 依赖性棘密度增加的可观性,又表明了相对稳定的浅层皮质回路的区域和树突选择性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/b42354b40ba3/fncel-07-00062-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/c2a23fdeb7be/fncel-07-00062-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/5533b15df484/fncel-07-00062-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/9537afac9855/fncel-07-00062-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/ff3d7ad228ec/fncel-07-00062-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/b42354b40ba3/fncel-07-00062-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/c2a23fdeb7be/fncel-07-00062-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/5533b15df484/fncel-07-00062-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/9537afac9855/fncel-07-00062-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/ff3d7ad228ec/fncel-07-00062-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cf2/3661998/b42354b40ba3/fncel-07-00062-g005.jpg

相似文献

1
Rho GTPase-dependent plasticity of dendritic spines in the adult brain.树突棘在成年大脑中的 Rho GTPase 依赖性可塑性。
Front Cell Neurosci. 2013 May 23;7:62. doi: 10.3389/fncel.2013.00062. eCollection 2013.
2
Pyramidal Neurons in Different Cortical Layers Exhibit Distinct Dynamics and Plasticity of Apical Dendritic Spines.不同皮层层中的锥体神经元表现出树突棘顶端的不同动态和可塑性。
Front Neural Circuits. 2017 Jun 19;11:43. doi: 10.3389/fncir.2017.00043. eCollection 2017.
3
[Development of neuronal structure in the hippocampus during pre- and post-natal ontogenesis in the albino rat. III. Morphometric determination of ontogenetic changes in dendrite structure and spine distribution on pyramidal neurons (CA1) of the hippocampus].[白化大鼠出生前和出生后海马神经元结构的发育。III. 海马锥体神经元(CA1)树突结构和棘分布个体发育变化的形态计量学测定]
J Hirnforsch. 1976;17(3):255-75.
4
Perinatal undernutrition attenuates field excitatory postsynaptic potentials and influences dendritic spine density and morphology in hippocampus of male rat offspring.围产期营养不良可减弱海马体中兴奋性突触后电位,并影响雄性仔鼠海马的树突棘密度和形态。
Neuroscience. 2013 Aug 6;244:31-41. doi: 10.1016/j.neuroscience.2013.03.061. Epub 2013 Apr 6.
5
Inhibition of Rho via Arg and p190RhoGAP in the postnatal mouse hippocampus regulates dendritic spine maturation, synapse and dendrite stability, and behavior.通过精氨酸和p190RhoGAP抑制出生后小鼠海马体中的Rho可调节树突棘成熟、突触和树突稳定性以及行为。
J Neurosci. 2007 Oct 10;27(41):10982-92. doi: 10.1523/JNEUROSCI.0793-07.2007.
6
The guanine nucleotide exchange factor (GEF) Asef2 promotes dendritic spine formation via Rac activation and spinophilin-dependent targeting.鸟嘌呤核苷酸交换因子(GEF)Asef2通过Rac激活和依赖亲棘蛋白的靶向作用促进树突棘形成。
J Biol Chem. 2015 Apr 17;290(16):10295-308. doi: 10.1074/jbc.M114.605543. Epub 2015 Mar 6.
7
Comparison of Golgi-Cox and Intracellular Loading of Lucifer Yellow for Dendritic Spine Density and Morphology Analysis in the Mouse Brain.高尔基染色和 Lucifer Yellow 内染法在分析小鼠脑内树突棘密度和形态中的比较。
Neuroscience. 2022 Aug 21;498:1-18. doi: 10.1016/j.neuroscience.2022.06.029. Epub 2022 Jun 23.
8
Activation of Rho GTPases triggers structural remodeling and functional plasticity in the adult rat visual cortex.Rho GTPases 的激活触发成年大鼠视觉皮层的结构重塑和功能可塑性。
J Neurosci. 2011 Oct 19;31(42):15163-72. doi: 10.1523/JNEUROSCI.2617-11.2011.
9
Maternal Loss of Ube3a Impairs Experience-Driven Dendritic Spine Maintenance in the Developing Visual Cortex.母体Ube3a缺失会损害发育中的视觉皮层中经验驱动的树突棘维持。
J Neurosci. 2016 Apr 27;36(17):4888-94. doi: 10.1523/JNEUROSCI.4204-15.2016.
10
Control of synapse development and plasticity by Rho GTPase regulatory proteins.Rho GTPase 调节蛋白对突触发育和可塑性的控制。
Prog Neurobiol. 2011 Jul;94(2):133-48. doi: 10.1016/j.pneurobio.2011.04.011. Epub 2011 Apr 22.

引用本文的文献

1
Role of Serotonylation and SERT Posttranslational Modifications in Alzheimer's Disease Pathogenesis.血清素化和5-羟色胺转运体(SERT)的翻译后修饰在阿尔茨海默病发病机制中的作用
Aging Dis. 2024 Mar 28;16(2):841-858. doi: 10.14336/AD.2024.0328.
2
Delta-Catenin as a Modulator of Rho GTPases in Neurons.δ-连环蛋白作为神经元中Rho GTP酶的调节剂
Front Cell Neurosci. 2022 Jul 4;16:939143. doi: 10.3389/fncel.2022.939143. eCollection 2022.
3
A direct interaction between RhoGDIα/Tau alleviates hyperphosphorylation of Tau in Alzheimer's disease and vascular dementia.

本文引用的文献

1
Rac1 selective activation improves retina ganglion cell survival and regeneration.Rac1 选择性激活可提高视网膜神经节细胞的存活率和再生能力。
PLoS One. 2013 May 29;8(5):e64350. doi: 10.1371/journal.pone.0064350. Print 2013.
2
Two-photon microscopy imaging of thy1GFP-M transgenic mice: a novel animal model to investigate brain dendritic cell subsets in vivo.双光子显微镜成像技术在 Thy1-GFP-M 转基因小鼠中的应用:一种新型动物模型,用于体内研究脑树突状细胞亚群。
PLoS One. 2013;8(2):e56144. doi: 10.1371/journal.pone.0056144. Epub 2013 Feb 7.
3
Behavioral effects of Rho GTPase modulation in a model of Alzheimer's disease.
RhoGDIα与Tau之间的直接相互作用可减轻阿尔茨海默病和血管性痴呆中Tau的过度磷酸化。
J Neuroimmune Pharmacol. 2023 Jun;18(1-2):58-71. doi: 10.1007/s11481-021-10049-w. Epub 2022 Jan 26.
4
The Cytotoxic Necrotizing Factors (CNFs)-A Family of Rho GTPase-Activating Bacterial Exotoxins.细胞毒性坏死因子(CNFs)-一类 Rho GTPase 激活细菌外毒素。
Toxins (Basel). 2021 Dec 15;13(12):901. doi: 10.3390/toxins13120901.
5
Environmental Enrichment Induces Epigenomic and Genome Organization Changes Relevant for Cognition.环境富集诱导与认知相关的表观基因组和基因组组织变化。
Front Mol Neurosci. 2021 May 5;14:664912. doi: 10.3389/fnmol.2021.664912. eCollection 2021.
6
MMP-9 Signaling Pathways That Engage Rho GTPases in Brain Plasticity.MMP-9 信号通路在大脑可塑性中涉及 Rho GTPases。
Cells. 2021 Jan 15;10(1):166. doi: 10.3390/cells10010166.
7
Roles of palmitoylation in structural long-term synaptic plasticity.棕榈酰化在结构长时程突触可塑性中的作用。
Mol Brain. 2021 Jan 11;14(1):8. doi: 10.1186/s13041-020-00717-y.
8
The Role of ADF/Cofilin in Synaptic Physiology and Alzheimer's Disease.肌动蛋白解聚因子/丝切蛋白在突触生理学及阿尔茨海默病中的作用
Front Cell Dev Biol. 2020 Nov 12;8:594998. doi: 10.3389/fcell.2020.594998. eCollection 2020.
9
Mutated RAP1GDS1 causes a new syndrome of dysmorphic feature, intellectual disability & speech delay.RAP1GDS1 基因突变导致一种新的综合征,表现为畸形特征、智力障碍和语言发育迟缓。
Ann Clin Transl Neurol. 2020 Jun;7(6):956-964. doi: 10.1002/acn3.51059. Epub 2020 May 19.
10
Transglutaminase in Receptor and Neurotransmitter-Regulated Functions.转谷氨酰胺酶在受体和神经递质调节功能中的作用
Med One. 2018;3(6). doi: 10.20900/mo.20180012. Epub 2018 Dec 5.
Rho GTPase 调节在阿尔茨海默病模型中的行为效应。
Behav Brain Res. 2013 Jan 15;237:223-9. doi: 10.1016/j.bbr.2012.09.043. Epub 2012 Sep 28.
4
Protocadherin clusters and cell adhesion kinase regulate dendrite complexity through Rho GTPase.原钙黏蛋白簇和细胞黏附激酶通过 Rho GTPase 调节树突复杂性。
J Mol Cell Biol. 2012 Dec;4(6):362-76. doi: 10.1093/jmcb/mjs034. Epub 2012 Jun 21.
5
Long-lasting efficacy of the cognitive enhancer cytotoxic necrotizing factor 1.认知增强剂细胞毒性坏死因子 1 的长效疗效。
Neuropharmacology. 2013 Jan;64:74-80. doi: 10.1016/j.neuropharm.2012.05.031. Epub 2012 May 31.
6
CNF1 improves astrocytic ability to support neuronal growth and differentiation in vitro.CNF1 可增强星形胶质细胞在体外支持神经元生长和分化的能力。
PLoS One. 2012;7(4):e34115. doi: 10.1371/journal.pone.0034115. Epub 2012 Apr 16.
7
Chronic pharmacological mGlu5 inhibition corrects fragile X in adult mice.慢性药理学 mGlu5 抑制可纠正成年小鼠的脆性 X 。
Neuron. 2012 Apr 12;74(1):49-56. doi: 10.1016/j.neuron.2012.03.009.
8
Cdc42: an important regulator of neuronal morphology.Cdc42:神经元形态的重要调节因子。
Int J Biochem Cell Biol. 2012 Mar;44(3):447-51. doi: 10.1016/j.biocel.2011.11.022. Epub 2011 Dec 8.
9
Modulation of RhoGTPases improves the behavioral phenotype and reverses astrocytic deficits in a mouse model of Rett syndrome.RhoGTPases 的调节改善了雷特综合征小鼠模型的行为表型并逆转了星形胶质细胞缺陷。
Neuropsychopharmacology. 2012 Apr;37(5):1152-63. doi: 10.1038/npp.2011.301. Epub 2011 Dec 7.
10
Activation of Rho GTPases triggers structural remodeling and functional plasticity in the adult rat visual cortex.Rho GTPases 的激活触发成年大鼠视觉皮层的结构重塑和功能可塑性。
J Neurosci. 2011 Oct 19;31(42):15163-72. doi: 10.1523/JNEUROSCI.2617-11.2011.