• 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

脊髓性肌萎缩症小鼠模型中运动神经元和感觉神经元的不同及重叠性改变

Distinct and overlapping alterations in motor and sensory neurons in a mouse model of spinal muscular atrophy.

作者信息

Jablonka Sibylle, Karle Kathrin, Sandner Beatrice, Andreassi Catia, von Au Katja, Sendtner Michael

机构信息

Institute for Clinical Neurobiology, Josef-Schneider-Str. 11, D-97080 Wuerzburg, Germany.

出版信息

Hum Mol Genet. 2006 Feb 1;15(3):511-8. doi: 10.1093/hmg/ddi467. Epub 2006 Jan 5.

DOI:10.1093/hmg/ddi467
PMID:16396995
Abstract

Motor neuron degeneration is the predominant pathological feature of spinal muscular atrophy (SMA). In patients with severe forms of the disease, additional sensory abnormalities have been reported. However, it is not clear whether the loss of sensory neurons is a common feature in severe forms of the disease, how many neurons are lost and how loss of sensory neurons compares with motor neuron degeneration. We have analysed dorsal root ganglionic sensory neurons in Smn-/-;SMN2 mice, a model of type I SMA. In contrast to lumbar motor neurons, no loss of sensory neurons in the L5 dorsal root ganglia is found at post-natal days 3-5 when these mice are severely paralyzed and die from motor defects. Survival of cultured sensory neurons in the presence of NGF and other neurotrophic factors is not reduced in comparison to wild-type controls. However, isolated sensory neurons have shorter neurites and smaller growth cones, and beta-actin protein and beta-actin mRNA are reduced in sensory neurite terminals. In footpads of Smn-deficient mouse embryos, sensory nerve terminals are smaller, suggesting that Smn deficiency reduces neurite outgrowth during embryogenesis. These data indicate that pathological alterations in severe forms of SMA are not restricted to motor neurons, but the defects in the sensory neurons are milder than those in the motor neurons.

摘要

运动神经元变性是脊髓性肌萎缩症(SMA)的主要病理特征。在患有严重形式该疾病的患者中,已有额外感觉异常的报道。然而,尚不清楚感觉神经元的丧失是否是严重形式疾病的常见特征、有多少神经元丧失以及感觉神经元的丧失与运动神经元变性相比情况如何。我们分析了I型SMA模型Smn-/-;SMN2小鼠的背根神经节感觉神经元。与腰段运动神经元不同,在出生后3 - 5天,当这些小鼠严重瘫痪并死于运动缺陷时,未发现L5背根神经节中的感觉神经元有丧失。与野生型对照相比,在存在神经生长因子(NGF)和其他神经营养因子的情况下,培养的感觉神经元的存活率并未降低。然而,分离出的感觉神经元的神经突较短且生长锥较小,并且感觉神经突末端的β-肌动蛋白蛋白和β-肌动蛋白mRNA减少。在Smn缺陷型小鼠胚胎的足垫中,感觉神经末梢较小,这表明Smn缺陷会减少胚胎发育过程中的神经突生长。这些数据表明,严重形式SMA的病理改变并不局限于运动神经元,而是感觉神经元中的缺陷比运动神经元中的缺陷更轻微。

相似文献

1
Distinct and overlapping alterations in motor and sensory neurons in a mouse model of spinal muscular atrophy.脊髓性肌萎缩症小鼠模型中运动神经元和感觉神经元的不同及重叠性改变
Hum Mol Genet. 2006 Feb 1;15(3):511-8. doi: 10.1093/hmg/ddi467. Epub 2006 Jan 5.
2
A role for complexes of survival of motor neurons (SMN) protein with gemins and profilin in neurite-like cytoplasmic extensions of cultured nerve cells.运动神经元存活蛋白(SMN)与双微体蛋白及丝切蛋白复合物在培养神经细胞的类神经突细胞质延伸中的作用。
Exp Cell Res. 2005 Sep 10;309(1):185-97. doi: 10.1016/j.yexcr.2005.05.014.
3
Smn, the spinal muscular atrophy-determining gene product, modulates axon growth and localization of beta-actin mRNA in growth cones of motoneurons.生存运动神经元蛋白(Smn)是脊髓性肌萎缩症的决定性基因产物,可调节运动神经元生长锥中轴突的生长以及β-肌动蛋白信使核糖核酸(β-actin mRNA)的定位。
J Cell Biol. 2003 Nov 24;163(4):801-12. doi: 10.1083/jcb.200304128. Epub 2003 Nov 17.
4
Characterization of Ighmbp2 in motor neurons and implications for the pathomechanism in a mouse model of human spinal muscular atrophy with respiratory distress type 1 (SMARD1).运动神经元中Ighmbp2的特征及其对1型呼吸窘迫型人类脊髓性肌萎缩症(SMARD1)小鼠模型发病机制的影响
Hum Mol Genet. 2004 Sep 15;13(18):2031-42. doi: 10.1093/hmg/ddh222. Epub 2004 Jul 21.
5
The survival of motor neurons protein determines the capacity for snRNP assembly: biochemical deficiency in spinal muscular atrophy.运动神经元存活蛋白决定了小核核糖核蛋白组装的能力:脊髓性肌萎缩症中的生化缺陷。
Mol Cell Biol. 2005 Jul;25(13):5543-51. doi: 10.1128/MCB.25.13.5543-5551.2005.
6
The SMN binding protein Gemin2 is not involved in motor axon outgrowth.运动神经元存活蛋白结合蛋白Gemin2不参与运动轴突的生长。
Dev Neurobiol. 2008 Feb 1;68(2):182-94. doi: 10.1002/dneu.20582.
7
Stat5 constitutive activation rescues defects in spinal muscular atrophy.Stat5组成性激活可挽救脊髓性肌萎缩症的缺陷。
Hum Mol Genet. 2007 Mar 1;16(5):499-514. doi: 10.1093/hmg/ddl482. Epub 2007 Jan 12.
8
Spinal muscular atrophy: a deficiency in a ubiquitous protein; a motor neuron-specific disease.脊髓性肌萎缩症:一种普遍存在的蛋白质缺乏症;一种运动神经元特异性疾病。
Neuron. 2005 Dec 22;48(6):885-96. doi: 10.1016/j.neuron.2005.12.001.
9
Is good housekeeping the key to motor neuron survival?良好的细胞内环境稳态是运动神经元存活的关键吗?
Cell. 2008 May 16;133(4):572-4. doi: 10.1016/j.cell.2008.05.002.
10
Activation of RNA metabolism-related genes in mouse but not human tissues deficient in SMN.在缺乏生存运动神经元(SMN)的小鼠而非人类组织中,与RNA代谢相关的基因被激活。
Physiol Genomics. 2006 Jan 12;24(2):97-104. doi: 10.1152/physiolgenomics.00134.2005. Epub 2005 Aug 23.

引用本文的文献

1
Comorbidities in spinal muscular atrophy and their impact on the course of the underlying disease: a real-life observational study.脊髓性肌萎缩症的合并症及其对基础疾病病程的影响:一项真实世界观察性研究
BMC Musculoskelet Disord. 2025 Sep 2;26(1):839. doi: 10.1186/s12891-025-09133-6.
2
Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications.脊髓性肌萎缩症中的神经胶质细胞:关于非细胞自主机制及治疗意义的推测
Neurol Int. 2025 Mar 13;17(3):41. doi: 10.3390/neurolint17030041.
3
PRMT inhibitor promotes SMN2 exon 7 inclusion and synergizes with nusinersen to rescue SMA mice.
PRMT 抑制剂促进 SMN2 外显子 7 的包含,并与 nusinersen 协同作用,拯救 SMA 小鼠。
EMBO Mol Med. 2023 Nov 8;15(11):e17683. doi: 10.15252/emmm.202317683. Epub 2023 Sep 19.
4
Cerebellar structural, astrocytic, and neuronal abnormalities in the SMNΔ7 mouse model of spinal muscular atrophy.脊髓性肌萎缩症 SMNΔ7 小鼠模型中的小脑结构、星形胶质细胞和神经元异常。
Brain Pathol. 2023 Sep;33(5):e13162. doi: 10.1111/bpa.13162. Epub 2023 May 22.
5
Ultrastructural characterization of peripheral denervation in a mouse model of Type III spinal muscular atrophy.III 型脊肌萎缩症小鼠模型周围去神经的超微结构特征。
J Neural Transm (Vienna). 2021 Jun;128(6):771-791. doi: 10.1007/s00702-021-02353-9. Epub 2021 May 17.
6
Spinal muscular atrophy: Broad disease spectrum and sex-specific phenotypes.脊髓性肌萎缩症:广泛的疾病谱和性别特异性表型。
Biochim Biophys Acta Mol Basis Dis. 2021 Apr 1;1867(4):166063. doi: 10.1016/j.bbadis.2020.166063. Epub 2021 Jan 5.
7
The Small-Molecule Flunarizine in Spinal Muscular Atrophy Patient Fibroblasts Impacts on the Gemin Components of the SMN Complex and TDP43, an RNA-Binding Protein Relevant to Motor Neuron Diseases.小分子氟桂利嗪对脊髓性肌萎缩症患者成纤维细胞中运动神经元疾病相关RNA结合蛋白TDP43及SMN复合物的双子组件产生影响。
Front Mol Biosci. 2020 Apr 17;7:55. doi: 10.3389/fmolb.2020.00055. eCollection 2020.
8
SMN deficiency causes pain hypersensitivity in a mild SMA mouse model through enhancing excitability of nociceptive dorsal root ganglion neurons.运动神经元存活基因(SMN)缺失通过增强伤害感受性背根神经节神经元的兴奋性,引起轻度脊髓性肌萎缩症(SMA)小鼠模型的痛觉过敏。
Sci Rep. 2019 Apr 24;9(1):6493. doi: 10.1038/s41598-019-43053-5.
9
Molecular Mechanisms Underlying Sensory-Motor Circuit Dysfunction in SMA.脊髓性肌萎缩症中感觉运动回路功能障碍的分子机制
Front Mol Neurosci. 2019 Mar 4;12:59. doi: 10.3389/fnmol.2019.00059. eCollection 2019.
10
Challenges and Future Prospects on 3D Modeling of the Neuromuscular Circuit.神经肌肉回路三维建模的挑战与未来前景
Front Bioeng Biotechnol. 2018 Dec 11;6:194. doi: 10.3389/fbioe.2018.00194. eCollection 2018.