• 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

相似文献

1
Agenesis of the corpus callosum in Nogo receptor deficient mice.Nogo受体缺陷小鼠的胼胝体发育不全
J Comp Neurol. 2017 Feb 1;525(2):291-301. doi: 10.1002/cne.24064. Epub 2016 Jul 8.
2
Multiple Slits regulate the development of midline glial populations and the corpus callosum.多裂隙调节中线胶质细胞群体和胼胝体的发育。
Dev Biol. 2012 May 1;365(1):36-49. doi: 10.1016/j.ydbio.2012.02.004. Epub 2012 Feb 11.
3
Defects in neural guidepost structures and failure to remove leptomeningeal cells from the septal midline behind the interhemispheric fusion defects in Netrin1 deficient mice.Netrin1基因缺陷小鼠中,神经引导结构存在缺陷,且在半球间融合缺陷后方的中隔中线处未能清除软脑膜细胞。
Int J Dev Neurosci. 2015 Dec;47(Pt B):206-15. doi: 10.1016/j.ijdevneu.2015.08.005. Epub 2015 Oct 22.
4
PlexinA1 is crucial for the midline crossing of callosal axons during corpus callosum development in BALB/cAJ mice.PlexinA1 对于 BALB/cAJ 小鼠胼胝体发育过程中胼胝体轴突的中线穿越是至关重要的。
PLoS One. 2019 Aug 20;14(8):e0221440. doi: 10.1371/journal.pone.0221440. eCollection 2019.
5
Abnormal development of forebrain midline glia and commissural projections in Nfia knock-out mice.Nfia基因敲除小鼠前脑中线神经胶质细胞和连合投射的异常发育。
J Neurosci. 2003 Jan 1;23(1):203-12. doi: 10.1523/JNEUROSCI.23-01-00203.2003.
6
Axonal pathfinding mechanisms at the cortical midline and in the development of the corpus callosum.皮质中线处的轴突导向机制与胼胝体的发育
Braz J Med Biol Res. 2002 Dec;35(12):1431-9. doi: 10.1590/s0100-879x2002001200004.
7
The tumor suppressor Nf2 regulates corpus callosum development by inhibiting the transcriptional coactivator Yap.肿瘤抑制因子Nf2通过抑制转录共激活因子Yap来调节胼胝体发育。
Development. 2014 Nov;141(21):4182-93. doi: 10.1242/dev.111260.
8
Gli3 controls corpus callosum formation by positioning midline guideposts during telencephalic patterning.Gli3 通过在端脑模式形成过程中定位中线导引来控制胼胝体的形成。
Cereb Cortex. 2014 Jan;24(1):186-98. doi: 10.1093/cercor/bhs303. Epub 2012 Oct 4.
9
Perinatal midline astrocyte development is impaired in fibroblast growth factor 8 hypomorphic mice.成纤维细胞生长因子8低表达小鼠的围产期中线星形胶质细胞发育受损。
Brain Res. 2016 Sep 1;1646:287-296. doi: 10.1016/j.brainres.2016.06.015. Epub 2016 Jun 9.
10
Agenesis of the Corpus Callosum Due to Defective Glial Wedge Formation in Lhx2 Mutant Mice.Lhx2突变小鼠中由于神经胶质楔形形成缺陷导致的胼胝体发育不全
Cereb Cortex. 2015 Sep;25(9):2707-18. doi: 10.1093/cercor/bhu067. Epub 2014 Apr 29.

引用本文的文献

1
A selective defect in the glial wedge as part of the neuroepithelium disruption in hydrocephalus development in the mouse hyh model is associated with complete corpus callosum dysgenesis.在小鼠hyh模型中,作为脑积水发育过程中神经上皮破坏一部分的神经胶质楔形区的选择性缺陷与胼胝体完全发育不全有关。
Front Cell Neurosci. 2024 Feb 21;18:1330412. doi: 10.3389/fncel.2024.1330412. eCollection 2024.
2
DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation.DCC 调控星形胶质细胞发育对于端脑形态发生和胼胝体形成至关重要。
Elife. 2021 Apr 19;10:e61769. doi: 10.7554/eLife.61769.
3
Amelioration of the abnormal phenotype of a new L1 syndrome mouse mutation with L1 mimetics.用 L1 模拟物改善新型 L1 综合征小鼠突变的异常表型。
FASEB J. 2021 Feb;35(2):e21329. doi: 10.1096/fj.202002163R.
4
Corpus Callosum Agenesis: An Insight into the Etiology and Spectrum of Symptoms.胼胝体发育不全:对病因及症状谱的深入了解
Brain Sci. 2020 Sep 9;10(9):625. doi: 10.3390/brainsci10090625.
5
The autism- and schizophrenia-associated protein CYFIP1 regulates bilateral brain connectivity and behaviour.自闭症和精神分裂症相关蛋白 CYFIP1 调节左右脑连接和行为。
Nat Commun. 2019 Aug 1;10(1):3454. doi: 10.1038/s41467-019-11203-y.
6
Germline Chd8 haploinsufficiency alters brain development in mouse.生殖系Chd8单倍剂量不足会改变小鼠的大脑发育。
Nat Neurosci. 2017 Aug;20(8):1062-1073. doi: 10.1038/nn.4592. Epub 2017 Jun 26.

本文引用的文献

1
Non-canonical actions of Nogo-A and its receptors.Nogo-A 及其受体的非经典作用。
Biochem Pharmacol. 2016 Jan 15;100:28-39. doi: 10.1016/j.bcp.2015.08.113. Epub 2015 Sep 4.
2
PlexinA1 is a new Slit receptor and mediates axon guidance function of Slit C-terminal fragments.PlexinA1 是一种新的 Slit 受体,介导 Slit C 末端片段的轴突导向功能。
Nat Neurosci. 2015 Jan;18(1):36-45. doi: 10.1038/nn.3893. Epub 2014 Dec 8.
3
An RNA-sequencing transcriptome and splicing database of glia, neurons, and vascular cells of the cerebral cortex.大脑皮层神经胶质细胞、神经元和血管细胞的 RNA 测序转录组和剪接数据库。
J Neurosci. 2014 Sep 3;34(36):11929-47. doi: 10.1523/JNEUROSCI.1860-14.2014.
4
Netrin-DCC signaling regulates corpus callosum formation through attraction of pioneering axons and by modulating Slit2-mediated repulsion.Netrin-DCC 信号通过吸引先驱轴突并调节 Slit2 介导的排斥作用来调节胼胝体的形成。
Cereb Cortex. 2014 May;24(5):1138-51. doi: 10.1093/cercor/bhs395. Epub 2013 Jan 9.
5
NgR1 and NgR3 are receptors for chondroitin sulfate proteoglycans.NgR1 和 NgR3 是软骨素蛋白聚糖的受体。
Nat Neurosci. 2012 Mar 11;15(5):703-12. doi: 10.1038/nn.3070.
6
In vivo evidence that TRAF4 is required for central nervous system myelin homeostasis.体内证据表明 TRAF4 对于中枢神经系统髓鞘的稳态维持是必需的。
PLoS One. 2012;7(2):e30917. doi: 10.1371/journal.pone.0030917. Epub 2012 Feb 17.
7
Multiple Slits regulate the development of midline glial populations and the corpus callosum.多裂隙调节中线胶质细胞群体和胼胝体的发育。
Dev Biol. 2012 May 1;365(1):36-49. doi: 10.1016/j.ydbio.2012.02.004. Epub 2012 Feb 11.
8
The nogo receptor family restricts synapse number in the developing hippocampus.神经生长抑制因子受体家族限制发育中海马突触数量。
Neuron. 2012 Feb 9;73(3):466-81. doi: 10.1016/j.neuron.2011.11.029.
9
The Nogo-66 receptor family in the intact and diseased CNS.完整及病变中枢神经系统中的 Nogo-66 受体家族。
Cell Tissue Res. 2012 Jul;349(1):105-17. doi: 10.1007/s00441-012-1332-9. Epub 2012 Feb 8.
10
Noggin protects against ischemic brain injury in rodents.Noggin 可保护啮齿动物免受缺血性脑损伤。
Stroke. 2010 Feb;41(2):357-62. doi: 10.1161/STROKEAHA.109.565523. Epub 2009 Dec 17.

Nogo受体缺陷小鼠的胼胝体发育不全

Agenesis of the corpus callosum in Nogo receptor deficient mice.

作者信息

Yoo Seung-Wan, Motari Mary G, Schnaar Ronald L

机构信息

Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, 21205.

Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205.

出版信息

J Comp Neurol. 2017 Feb 1;525(2):291-301. doi: 10.1002/cne.24064. Epub 2016 Jul 8.

DOI:10.1002/cne.24064
PMID:27339102
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5138123/
Abstract

The corpus callosum (CC) is the largest fiber tract in the mammalian brain, linking the bilateral cerebral hemispheres. CC development depends on the proper balance of axon growth cone attractive and repellent cues leading axons to the midline and then directing them to the contralateral hemisphere. Imbalance of these cues results in CC agenesis or dysgenesis. Nogo receptors (NgR1, NgR2, and NgR3) are growth cone directive molecules known for inhibiting axon regeneration after injury. We report that mice lacking Nogo receptors (NgR123-null mice) display complete CC agenesis due to axon misdirection evidenced by ectopic axons including cortical Probst bundles. Because glia and glial-derived growth cone repellent factors (especially the diffusible factor Slit2) are required for CC development, their distribution was studied. Compared with wild-type mice, NgR123-null mice had a sharp increase in the glial marker glial fibrillary acidic protein (GFAP) and in Slit2 at the glial wedge and indusium griseum, midline structures required for CC formation. NgR123-null mice displayed reduced motor coordination and hyperactivity. These data are consistent with the hypotheses that Nogo receptors are membrane-bound growth cone repellent factors required for migration of axons across the midline at the CC, and that their absence results directly or indirectly in midline gliosis, increased Slit2, and complete CC agenesis. J. Comp. Neurol. 525:291-301, 2017. © 2016 Wiley Periodicals, Inc.

摘要

胼胝体(CC)是哺乳动物大脑中最大的纤维束,连接双侧大脑半球。CC的发育取决于轴突生长锥吸引和排斥信号的适当平衡,这些信号引导轴突到达中线,然后将它们导向对侧半球。这些信号的失衡会导致CC发育不全或发育异常。Nogo受体(NgR1、NgR2和NgR3)是生长锥导向分子,以抑制损伤后的轴突再生而闻名。我们报告,缺乏Nogo受体的小鼠(NgR123基因敲除小鼠)表现出完全的CC发育不全,这是由于轴突误向导致的,异位轴突包括皮质普罗布斯特束可证明这一点。由于胶质细胞和胶质细胞衍生的生长锥排斥因子(尤其是可扩散因子Slit2)是CC发育所必需的,因此研究了它们的分布。与野生型小鼠相比,NgR123基因敲除小鼠在胶质楔和灰被(CC形成所需的中线结构)处的胶质细胞标志物胶质纤维酸性蛋白(GFAP)和Slit2急剧增加。NgR123基因敲除小鼠表现出运动协调性降低和多动。这些数据与以下假设一致:Nogo受体是轴突在CC处跨越中线迁移所需的膜结合生长锥排斥因子,其缺失直接或间接导致中线胶质增生、Slit2增加和完全的CC发育不全。《比较神经学杂志》525:291 - 301,2017年。©2016威利期刊公司。