• 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

神经退行性疾病中对兴奋性氨基酸诱导毒性的差异易感性和选择性神经元丢失。

Differential vulnerability to excitatory amino acid-induced toxicity and selective neuronal loss in neurodegenerative diseases.

作者信息

Weiss J H, Choi D W

机构信息

Department of Neurology, Stanford University Medical Centre, California 94305.

出版信息

Can J Neurol Sci. 1991 Aug;18(3 Suppl):394-7. doi: 10.1017/s0317167100032522.

DOI:10.1017/s0317167100032522
PMID:1657348
Abstract

Neurodegenerative diseases are characterized by selective degeneration of certain biochemically distinct subpopulations of central neurons. Studies of the intrinsic vulnerability of such neurons to injury by excitatory amino acids in vitro, as well as study of neurologic syndromes produced in animals or humans by ingestion of environmental excitatory amino acid neurotoxins may suggest a link between excitotoxicity, and the pathogenesis of certain neurodegenerative diseases.

摘要

神经退行性疾病的特征是中枢神经元中某些生物化学性质不同的亚群选择性退化。对这类神经元在体外对兴奋性氨基酸损伤的内在易损性的研究，以及对动物或人类因摄入环境兴奋性氨基酸神经毒素而产生的神经综合征的研究，可能提示兴奋性毒性与某些神经退行性疾病的发病机制之间存在联系。

相似文献

1
Differential vulnerability to excitatory amino acid-induced toxicity and selective neuronal loss in neurodegenerative diseases.神经退行性疾病中对兴奋性氨基酸诱导毒性的差异易感性和选择性神经元丢失。
Can J Neurol Sci. 1991 Aug;18(3 Suppl):394-7. doi: 10.1017/s0317167100032522.
2
Metabotropic glutamate receptors and neuronal toxicity.代谢型谷氨酸受体与神经元毒性。
Adv Exp Med Biol. 1992;318:137-45. doi: 10.1007/978-1-4615-3426-6_12.
3
Calcium and glutamate-induced cortical neuronal death.
Res Publ Assoc Res Nerv Ment Dis. 1993;71:23-34.
4
Activation of the metabotropic glutamate receptor attenuates N-methyl-D-aspartate neurotoxicity in cortical cultures.代谢型谷氨酸受体的激活可减轻皮层培养物中的N-甲基-D-天冬氨酸神经毒性。
Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9431-5. doi: 10.1073/pnas.88.21.9431.
5
Excitatory amino acid receptors and disease.兴奋性氨基酸受体与疾病
Curr Opin Neurol Neurosurg. 1992 Aug;5(4):508-13.
6
Involvement of three glutamate receptor epsilon subunits in the formation of N-methyl-D-aspartate receptors mediating excitotoxicity in primary cultures of mouse cerebellar granule cells.三种谷氨酸受体ε亚基参与介导小鼠小脑颗粒细胞原代培养物中兴奋性毒性的N-甲基-D-天冬氨酸受体的形成。
Neuroscience. 1997 Jun;78(4):1129-46. doi: 10.1016/s0306-4522(96)00630-6.
7
Cortical neurons containing calretinin are selectively resistant to calcium overload and excitotoxicity in vitro.含有钙视网膜蛋白的皮质神经元在体外对钙超载和兴奋性毒性具有选择性抗性。
Neuroscience. 1994 Jul;61(2):307-16. doi: 10.1016/0306-4522(94)90233-x.
8
Characterization of excitatory amino acid neurotoxicity in N-methyl-D-aspartate receptor-deficient mouse cortical neuronal cells.N-甲基-D-天冬氨酸受体缺陷型小鼠皮质神经元细胞中兴奋性氨基酸神经毒性的特征
Eur J Neurosci. 1996 Jan;8(1):69-78. doi: 10.1111/j.1460-9568.1996.tb01168.x.
9
N-methyl-D-aspartate receptor-mediated mitochondrial Ca(2+) overload in acute excitotoxic motor neuron death: a mechanism distinct from chronic neurotoxicity after Ca(2+) influx.N-甲基-D-天冬氨酸受体介导的线粒体Ca(2+)超载在急性兴奋性毒性运动神经元死亡中的作用：一种不同于Ca(2+)内流后慢性神经毒性的机制。
J Neurosci Res. 2001 Mar 1;63(5):377-87. doi: 10.1002/1097-4547(20010301)63:5<377::AID-JNR1032>3.0.CO;2-#.
10
Excitotoxicity and neurodegenerative diseases.
Curr Opin Neurol. 1995 Dec;8(6):487-97. doi: 10.1097/00019052-199512000-00017.

引用本文的文献

1
The Crosstalk Between Ferritinophagy and Ferroptosis in Ischemic Stroke: Regulatory Mechanisms and Therapeutic Implications.缺血性脑卒中中铁自噬与铁死亡之间的相互作用：调控机制及治疗意义
Cell Mol Neurobiol. 2025 Jul 20;45(1):73. doi: 10.1007/s10571-025-01593-7.
2
Targeting mitochondrial Ca uptake for the treatment of amyotrophic lateral sclerosis.靶向线粒体钙摄取治疗肌萎缩侧索硬化症。
J Physiol. 2024 Apr;602(8):1519-1549. doi: 10.1113/JP284143. Epub 2023 Nov 27.
3
Altered mRNA editing and expression of ionotropic glutamate receptors after kainic acid exposure in cyclooxygenase-2 deficient mice.
环氧合酶-2 缺陷型小鼠暴露于红藻氨酸后，离子型谷氨酸受体的 mRNA 编辑和表达改变。
PLoS One. 2011 May 12;6(5):e19398. doi: 10.1371/journal.pone.0019398.