• 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

实验性帕金森病纹状体突触变化:NMDA 受体在突触后致密物中的转运作用

Striatal synaptic changes in experimental parkinsonism: role of NMDA receptor trafficking in PSD.

作者信息

Picconi Barbara, Ghiglieri Veronica, Bagetta Vincenza, Barone Ilaria, Sgobio Carmelo, Calabresi Paolo

机构信息

Laboratorio di Neurofisiologia, Fondazione Santa Lucia, IRCCS c/o CERC, Via del Fosso di Fiorano 64, Rome, Italy.

出版信息

Parkinsonism Relat Disord. 2008;14 Suppl 2:S145-9. doi: 10.1016/j.parkreldis.2008.04.019. Epub 2008 Jun 25.

DOI:10.1016/j.parkreldis.2008.04.019
PMID:18583173
Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive degeneration of dopaminergic terminals from substantia nigra pars compacts, which leads to the motor symptoms observed in this disorder. L-Dopa administration represents the most effective therapeutic treatment of PD, but the development of disabling dyskinetic movements is a dramatic consequence of the treatment. The organization and functional interactions of glutamate receptors within the striatum appear to be crucial both in the pathogenesis of PD and in the development of dyskinesia. At the molecular level, it has become increasingly evident that the glutamatergic NMDA receptor complex is a dynamic structure that is involved in the regulation of corticostriatal long-term synaptic changes, which is altered in experimental PD and in dyskinesia.

摘要

帕金森病(PD)是一种神经退行性疾病,其特征是黑质致密部多巴胺能终末进行性退化,这导致了该疾病中出现的运动症状。左旋多巴给药是PD最有效的治疗方法,但致残性运动障碍的出现是该治疗的一个严重后果。纹状体内谷氨酸受体的组织和功能相互作用在PD的发病机制和运动障碍的发展中似乎都至关重要。在分子水平上,越来越明显的是,谷氨酸能N-甲基-D-天冬氨酸(NMDA)受体复合物是一种动态结构,参与皮质纹状体长期突触变化的调节,而在实验性PD和运动障碍中这种调节会发生改变。

相似文献

1
Striatal synaptic changes in experimental parkinsonism: role of NMDA receptor trafficking in PSD.实验性帕金森病纹状体突触变化:NMDA 受体在突触后致密物中的转运作用
Parkinsonism Relat Disord. 2008;14 Suppl 2:S145-9. doi: 10.1016/j.parkreldis.2008.04.019. Epub 2008 Jun 25.
2
Higher free D-aspartate and N-methyl-D-aspartate levels prevent striatal depotentiation and anticipate L-DOPA-induced dyskinesia.较高的游离 D-天冬氨酸和 N-甲基-D-天冬氨酸水平可阻止纹状体去极化,并可预测左旋多巴诱导的运动障碍。
Exp Neurol. 2011 Dec;232(2):240-50. doi: 10.1016/j.expneurol.2011.09.013. Epub 2011 Sep 17.
3
Loss of synaptic D1 dopamine/N-methyl-D-aspartate glutamate receptor complexes in L-DOPA-induced dyskinesia in the rat.大鼠左旋多巴诱导的异动症中突触多巴胺D1/谷氨酸N-甲基-D-天冬氨酸受体复合物的丧失
Mol Pharmacol. 2006 Mar;69(3):805-12. doi: 10.1124/mol.105.016667. Epub 2005 Dec 19.
4
Synaptic dysfunction in Parkinson's disease.帕金森病中的突触功能障碍。
Biochem Soc Trans. 2010 Apr;38(2):493-7. doi: 10.1042/BST0380493.
5
Levodopa-induced dyskinesia: a pathological form of striatal synaptic plasticity?左旋多巴诱发的异动症:一种纹状体突触可塑性的病理形式?
Ann Neurol. 2000 Apr;47(4 Suppl 1):S60-8; discussion S68-9.
6
Altered D(1) dopamine receptor trafficking in parkinsonian and dyskinetic non-human primates.帕金森病和异动症非人类灵长类动物中D(1)多巴胺受体转运的改变
Neurobiol Dis. 2007 May;26(2):452-63. doi: 10.1016/j.nbd.2007.02.001. Epub 2007 Feb 9.
7
Combined 5-HT1A and 5-HT1B receptor agonists for the treatment of L-DOPA-induced dyskinesia.联合5-HT1A和5-HT1B受体激动剂治疗左旋多巴诱导的运动障碍。
Brain. 2008 Dec;131(Pt 12):3380-94. doi: 10.1093/brain/awn235. Epub 2008 Oct 24.
8
The NR2B-selective NMDA receptor antagonist CP-101,606 exacerbates L-DOPA-induced dyskinesia and provides mild potentiation of anti-parkinsonian effects of L-DOPA in the MPTP-lesioned marmoset model of Parkinson's disease.NR2B 选择性 N-甲基-D-天冬氨酸(NMDA)受体拮抗剂 CP-101,606 会加剧左旋多巴诱导的运动障碍,并在帕金森病的 MPTP 损伤狨猴模型中对左旋多巴的抗帕金森病作用产生轻度增强效果。
Exp Neurol. 2004 Aug;188(2):471-9. doi: 10.1016/j.expneurol.2004.05.004.
9
l-DOPA dosage is critically involved in dyskinesia via loss of synaptic depotentiation.左旋多巴的剂量通过突触去增强作用的丧失与运动障碍密切相关。
Neurobiol Dis. 2008 Feb;29(2):327-35. doi: 10.1016/j.nbd.2007.10.001. Epub 2007 Oct 11.
10
Rabphilin 3A: A novel target for the treatment of levodopa-induced dyskinesias.Rabphilin 3A:左旋多巴诱导运动障碍治疗的新靶点。
Neurobiol Dis. 2017 Dec;108:54-64. doi: 10.1016/j.nbd.2017.08.001. Epub 2017 Aug 18.

引用本文的文献

1
Striatal spreading depolarization: Possible implication in levodopa-induced dyskinetic-like behavior.纹状体传播性去极化:可能与左旋多巴诱导的运动障碍样行为有关。
Mov Disord. 2019 Jun;34(6):832-844. doi: 10.1002/mds.27632. Epub 2019 Feb 13.
2
Mechanisms and Consequences of Dopamine Depletion-Induced Attenuation of the Spinophilin/Neurofilament Medium Interaction.多巴胺耗竭诱导的亲嗜素/中等神经丝相互作用减弱的机制及后果
Neural Plast. 2017;2017:4153076. doi: 10.1155/2017/4153076. Epub 2017 May 28.
3
Prion protein as a mediator of synaptic transmission.
朊病毒蛋白作为突触传递的介质。
Commun Integr Biol. 2015 Aug 14;8(4):e1063753. doi: 10.1080/19420889.2015.1063753. eCollection 2015 Jul-Aug.
4
Roles of Ca(2+)/calmodulin-dependent protein kinase II in subcellular expression of striatal N-methyl-D-aspartate receptors in l-3, 4-dihydroxyphenylalanine-induced dyskinetic rats.钙/钙调蛋白依赖性蛋白激酶II在L-3,4-二羟基苯丙氨酸诱导的异动症大鼠纹状体N-甲基-D-天冬氨酸受体亚细胞表达中的作用
Drug Des Devel Ther. 2015 Apr 13;9:2119-28. doi: 10.2147/DDDT.S73868. eCollection 2015.
5
Motor cortical plasticity in Parkinson's disease.帕金森病中的运动皮质可塑性
Front Neurol. 2013 Sep 4;4:128. doi: 10.3389/fneur.2013.00128.
6
Ischemic-LTP in striatal spiny neurons of both direct and indirect pathway requires the activation of D1-like receptors and NO/soluble guanylate cyclase/cGMP transmission.直接和间接通路纹状体棘神经元的缺血性长时程增强需要 D1 样受体的激活和 NO/可溶性鸟苷酸环化酶/cGMP 传递。
J Cereb Blood Flow Metab. 2013 Feb;33(2):278-86. doi: 10.1038/jcbfm.2012.167. Epub 2012 Nov 14.
7
Vascular endothelial growth factor is upregulated by L-dopa in the parkinsonian brain: implications for the development of dyskinesia.左旋多巴上调帕金森病脑中血管内皮生长因子:与运动障碍发展的关系。
Brain. 2011 Aug;134(Pt 8):2339-57. doi: 10.1093/brain/awr165. Epub 2011 Jul 19.
8
Neuroregeneration in neurodegenerative disorders.神经退行性疾病中的神经再生。
BMC Neurol. 2011 Jun 23;11:75. doi: 10.1186/1471-2377-11-75.
9
Impact of dendritic spine preservation in medium spiny neurons on dopamine graft efficacy and the expression of dyskinesias in parkinsonian rats.树突棘在中棘神经元中的保留对多巴胺移植疗效和帕金森病大鼠运动障碍表达的影响。
Eur J Neurosci. 2010 Feb;31(3):478-90. doi: 10.1111/j.1460-9568.2010.07077.x. Epub 2010 Jan 25.