• 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

体外红藻氨酸对大型、SMI-32(+)脊髓神经元的损伤是钙离子依赖性的。

In vitro kainate injury to large, SMI-32(+) spinal neurons is Ca2+ dependent.

作者信息

Carriedo S G, Yin H Z, Lamberta R, Weiss J H

机构信息

Department of Neurology, University of California Irvine 92717-4290, USA.

出版信息

Neuroreport. 1995 Apr 19;6(6):945-8. doi: 10.1097/00001756-199504190-00030.

DOI:10.1097/00001756-199504190-00030
PMID:7612889
Abstract

The non-phosphorylated neurofilament marker, SMI-32, identifies ventral horn motor neurons in spinal cord slice. We show here that SMI-32 marks a subset of spinal cord neurons in culture. Many of these neurons ('large SMI-32(+) neurons') have morphological characteristics of identified motor neurons in vitro: large cell body size (> 20 microns), extensive neuritic arborization and, generally, one particularly long process. These neurons are preferentially injured by brief (40 min) kainate exposures, but not by NMDA exposures. This rapidly triggered damage to large SMI-32(+) neurons is Ca2+ dependent. In addition, most of the SMI-32(+) neurons exhibit kainate-stimulated Co2+ uptake, a histochemical technique which marks neurons possessing Ca(2+)-permeable AMPA/kainate receptor-gated channels. The unusual vulnerability of large SMI-32(+) spinal neurons to kainate toxicity may result from rapid Ca2+ entry through Ca(2+)-permeable AMPA/kainate channels.

摘要

非磷酸化神经丝标志物SMI-32可识别脊髓切片中的腹角运动神经元。我们在此表明,SMI-32标记了培养中的一部分脊髓神经元。这些神经元中的许多(“大型SMI-32(+)神经元”)在体外具有已识别运动神经元的形态特征:细胞体大(>20微米)、广泛的神经分支,并且通常有一个特别长的突起。这些神经元优先受到短暂(40分钟)的海藻酸暴露损伤,但不受NMDA暴露损伤。这种对大型SMI-32(+)神经元的快速触发损伤是钙依赖性的。此外,大多数SMI-32(+)神经元表现出海藻酸刺激的钴摄取,这是一种组织化学技术,可标记具有钙通透性AMPA/海藻酸受体门控通道的神经元。大型SMI-32(+)脊髓神经元对海藻酸毒性的异常易感性可能是由于通过钙通透性AMPA/海藻酸通道的快速钙内流所致。

相似文献

1
In vitro kainate injury to large, SMI-32(+) spinal neurons is Ca2+ dependent.体外红藻氨酸对大型、SMI-32(+)脊髓神经元的损伤是钙离子依赖性的。
Neuroreport. 1995 Apr 19;6(6):945-8. doi: 10.1097/00001756-199504190-00030.
2
Motor neurons are selectively vulnerable to AMPA/kainate receptor-mediated injury in vitro.在体外,运动神经元对AMPA/海人酸受体介导的损伤具有选择性易感性。
J Neurosci. 1996 Jul 1;16(13):4069-79. doi: 10.1523/JNEUROSCI.16-13-04069.1996.
3
Ca2+ and in vitro kainate damage to cortical and hippocampal SMI-32(+) neurons.
Neuroreport. 1995 Mar 7;6(4):629-32. doi: 10.1097/00001756-199503000-00011.
4
Spinal cord neurons are vulnerable to rapidly triggered kainate neurotoxicity in vitro.
Brain Res. 1995 Aug 21;689(2):265-70. doi: 10.1016/0006-8993(95)00532-u.
5
Kainate injury to cultured basal forebrain cholinergic neurons is Ca2+ dependent.海人藻酸对培养的基底前脑胆碱能神经元的损伤是钙依赖性的。
Neuroreport. 1994 Jul 21;5(12):1477-80. doi: 10.1097/00001756-199407000-00017.
6
Glial cells potentiate kainate-induced neuronal death in a motoneuron-enriched spinal coculture system.在富含运动神经元的脊髓共培养系统中,神经胶质细胞增强了红藻氨酸诱导的神经元死亡。
Brain Res. 1998 Oct 5;807(1-2):1-10. doi: 10.1016/s0006-8993(98)00569-1.
7
Cobalt accumulation in neurons expressing ionotropic excitatory amino acid receptors in young rat spinal cord: morphology and distribution.钴在幼鼠脊髓中表达离子型兴奋性氨基酸受体的神经元中的蓄积:形态学与分布
J Comp Neurol. 1994 Jun 15;344(3):321-35. doi: 10.1002/cne.903440302.
8
SMI-32 antibody against non-phosphorylated neurofilaments identifies a subpopulation of cultured cortical neurons hypersensitive to kainate toxicity.针对非磷酸化神经丝的SMI-32抗体可识别对红藻氨酸毒性高度敏感的培养皮质神经元亚群。
Neurosci Lett. 1995 Jul 14;194(1-2):1-4. doi: 10.1016/0304-3940(95)11698-v.
9
Rapid Ca2+ entry through Ca2+-permeable AMPA/Kainate channels triggers marked intracellular Ca2+ rises and consequent oxygen radical production.通过钙离子通透型AMPA/海人酸受体通道的快速钙离子内流引发显著的细胞内钙离子浓度升高及随后的氧自由基生成。
J Neurosci. 1998 Oct 1;18(19):7727-38. doi: 10.1523/JNEUROSCI.18-19-07727.1998.
10
Ca2+ permeable AMPA/kainate channels permit rapid injurious Ca2+ entry.钙离子通透的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸/海人藻酸受体通道允许钙离子快速有害内流。
Neuroreport. 1995 May 30;6(8):1089-92. doi: 10.1097/00001756-199505300-00004.

引用本文的文献

1
Calcium Permeable-AMPA Receptors and Excitotoxicity in Neurological Disorders.钙通透性-AMPA 受体与神经退行性疾病中的兴奋性毒性
Front Neural Circuits. 2021 Aug 17;15:711564. doi: 10.3389/fncir.2021.711564. eCollection 2021.
2
Transport of BMAA into Neurons and Astrocytes by System x.BMAA 通过 System x 向神经元和星形胶质细胞的转运。
Neurotox Res. 2018 Jan;33(1):1-5. doi: 10.1007/s12640-017-9739-4. Epub 2017 May 3.
3
Effective gene expression in the rat dorsal root ganglia with a non-viral vector delivered via spinal nerve injection.
经脊柱神经注射的非病毒载体在大鼠背根神经节中的有效基因表达。
Sci Rep. 2016 Oct 17;6:35612. doi: 10.1038/srep35612.
4
Intrathecal infusion of BMAA induces selective motor neuron damage and astrogliosis in the ventral horn of the spinal cord.鞘内注射β-甲氨基-L-丙氨酸(BMAA)可诱导脊髓腹角选择性运动神经元损伤和星形胶质细胞增生。
Exp Neurol. 2014 Nov;261:1-9. doi: 10.1016/j.expneurol.2014.06.003. Epub 2014 Jun 8.
5
Mechanisms underlying cell death in ischemia-like damage to the rat spinal cord in vitro.体外大鼠脊髓类似缺血损伤中细胞死亡的机制。
Cell Death Dis. 2013 Jul 4;4(7):e707. doi: 10.1038/cddis.2013.237.
6
TNF-α triggers rapid membrane insertion of Ca(2+) permeable AMPA receptors into adult motor neurons and enhances their susceptibility to slow excitotoxic injury.TNF-α 触发 Ca(2+) 可渗透的 AMPA 受体在成年运动神经元中的快速膜插入,并增强其对缓慢兴奋性毒性损伤的易感性。
Exp Neurol. 2012 Dec;238(2):93-102. doi: 10.1016/j.expneurol.2012.08.004. Epub 2012 Aug 19.
7
Marked synergism between mutant SOD1 and glutamate transport inhibition in the induction of motor neuronal degeneration in spinal cord slice cultures.突变型 SOD1 与谷氨酸转运抑制在脊髓切片培养中诱导运动神经元变性的协同作用明显。
Brain Res. 2012 Apr 11;1448:153-62. doi: 10.1016/j.brainres.2012.02.005. Epub 2012 Feb 9.
8
Inhibitory synaptic regulation of motoneurons: a new target of disease mechanisms in amyotrophic lateral sclerosis.运动神经元的抑制性突触调节:肌萎缩侧索硬化症发病机制的新靶点。
Mol Neurobiol. 2012 Feb;45(1):30-42. doi: 10.1007/s12035-011-8217-x. Epub 2011 Nov 10.
9
Effect of prolonged riluzole exposure on cultured motoneurons in a mouse model of ALS.延长利鲁唑暴露对 ALS 小鼠模型培养运动神经元的影响。
J Neurophysiol. 2012 Jan;107(1):484-92. doi: 10.1152/jn.00714.2011. Epub 2011 Oct 19.
10
Glycine receptor channels in spinal motoneurons are abnormal in a transgenic mouse model of amyotrophic lateral sclerosis.脊髓运动神经元中的甘氨酸受体通道在肌萎缩侧索硬化症的转基因小鼠模型中异常。
J Neurosci. 2011 Feb 23;31(8):2815-27. doi: 10.1523/JNEUROSCI.2475-10.2011.