• 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

阿尔茨海默病中突触前和突触后谷氨酸能功能

Presynaptic and postsynaptic glutamatergic function in Alzheimer's disease.

作者信息

Cowburn R, Hardy J, Roberts P, Briggs R

机构信息

Department of Biochemistry and Molecular Biology, St. Mary's Hospital Medical School, London, U.K.

出版信息

Neurosci Lett. 1988 Mar 21;86(1):109-13. doi: 10.1016/0304-3940(88)90192-9.

DOI:10.1016/0304-3940(88)90192-9
PMID:2896322
Abstract

Sodium dependent D-aspartate and Ca2+/Cl-independent L-glutamate binding assays were used to assess the integrity of glutamate uptake sites and postsynaptic NMDA receptor levels in control and Alzheimer's disease temporal cortex. The number of glutamate uptake sites was significantly and substantially reduced in accordance with previous findings. However, NMDA receptor levels were unchanged. This finding suggests that glutamatergic presynaptic elements are severely reduced in Alzheimer's disease, whilst postsynaptic elements remain intact.

摘要

采用钠依赖性D-天冬氨酸和钙/氯非依赖性L-谷氨酸结合试验,评估对照和阿尔茨海默病颞叶皮质中谷氨酸摄取位点的完整性和突触后N-甲基-D-天冬氨酸(NMDA)受体水平。与之前的研究结果一致,谷氨酸摄取位点的数量显著且大幅减少。然而,NMDA受体水平未发生变化。这一发现表明,在阿尔茨海默病中,谷氨酸能突触前元件严重减少,而突触后元件保持完整。

相似文献

1
Presynaptic and postsynaptic glutamatergic function in Alzheimer's disease.阿尔茨海默病中突触前和突触后谷氨酸能功能
Neurosci Lett. 1988 Mar 21;86(1):109-13. doi: 10.1016/0304-3940(88)90192-9.
2
Regional distribution of pre- and postsynaptic glutamatergic function in Alzheimer's disease.阿尔茨海默病中突触前和突触后谷氨酸能功能的区域分布
Brain Res. 1988 Jun 14;452(1-2):403-7. doi: 10.1016/0006-8993(88)90048-0.
3
Regional changes in [3H]D-aspartate and [3H]TCP binding sites in Alzheimer's disease brains.阿尔茨海默病大脑中[3H]D-天冬氨酸和[3H]TCP结合位点的区域变化。
Brain Res. 1988 Oct 11;462(1):76-82. doi: 10.1016/0006-8993(88)90587-2.
4
Differential alterations of cortical glutamatergic binding sites in senile dementia of the Alzheimer type.阿尔茨海默型老年痴呆症中皮质谷氨酸能结合位点的差异性改变。
Proc Natl Acad Sci U S A. 1990 Feb;87(4):1352-6. doi: 10.1073/pnas.87.4.1352.
5
Reduced glycine stimulation of [3H]MK-801 binding in Alzheimer's disease.阿尔茨海默病中甘氨酸对[3H]MK-801结合的刺激作用减弱。
J Neurochem. 1989 Sep;53(3):698-704. doi: 10.1111/j.1471-4159.1989.tb11760.x.
6
Comparison of L-[3H]glutamate, D-[3H]aspartate, DL-[3H]AP5 and [3H]NMDA as ligands for NMDA receptors in crude postsynaptic densities from rat brain.L-[3H]谷氨酸、D-[3H]天冬氨酸、DL-[3H]AP5和[3H]N-甲基-D-天冬氨酸作为大鼠脑粗制突触后致密物中N-甲基-D-天冬氨酸受体配体的比较。
Eur J Pharmacol. 1987 Jan 20;133(3):291-300. doi: 10.1016/0014-2999(87)90025-2.
7
N-methyl-D-aspartate receptors and Alzheimer's disease.N-甲基-D-天冬氨酸受体与阿尔茨海默病
Neurobiol Aging. 1989 Sep-Oct;10(5):603-5; discussion 618-20. doi: 10.1016/0197-4580(89)90144-9.
8
Sodium dependent D-[3H]aspartate binding in cerebral cortex in patients with Alzheimer's and Parkinson's diseases.
Neurosci Lett. 1987 Aug 18;79(1-2):213-7. doi: 10.1016/0304-3940(87)90699-9.
9
Autoreceptor regulation of glutamate and aspartate release from slices of the hippocampal CA1 area.海马CA1区切片中谷氨酸和天冬氨酸释放的自受体调节。
J Neurochem. 1991 May;56(5):1647-55. doi: 10.1111/j.1471-4159.1991.tb02063.x.
10
Cellular uptake disguises action of L-glutamate on N-methyl-D-aspartate receptors. With an appendix: diffusion of transported amino acids into brain slices.细胞摄取掩盖了L-谷氨酸对N-甲基-D-天冬氨酸受体的作用。附有附录:转运氨基酸在脑片中的扩散。
Br J Pharmacol. 1985 May;85(1):297-307. doi: 10.1111/j.1476-5381.1985.tb08860.x.

引用本文的文献

1
Fueling Brain Inhibition: Integrating GABAergic Neurotransmission and Energy Metabolism.为大脑抑制提供能量:整合γ-氨基丁酸能神经传递与能量代谢
Neurochem Res. 2025 Apr 7;50(2):136. doi: 10.1007/s11064-025-04384-0.
2
The glutamatergic system in Alzheimer's disease: a systematic review with meta-analysis.阿尔茨海默病中的谷氨酸能系统:系统评价与荟萃分析。
Mol Psychiatry. 2024 Jul;29(7):2261-2273. doi: 10.1038/s41380-024-02473-0. Epub 2024 Feb 16.
3
TDP-43 promotes tau accumulation and selective neurotoxicity in bigenic Caenorhabditis elegans.
TDP-43 促进双转基因秀丽隐杆线虫中 tau 的积累和选择性神经毒性。
Dis Model Mech. 2022 Apr 1;15(4). doi: 10.1242/dmm.049323. Epub 2022 Apr 27.
4
Integrative genomic analysis of PPP3R1 in Alzheimer's disease: a potential biomarker for predictive, preventive, and personalized medical approach.阿尔茨海默病中PPP3R1的综合基因组分析:一种用于预测、预防和个性化医疗方法的潜在生物标志物。
EPMA J. 2021 Nov 15;12(4):647-658. doi: 10.1007/s13167-021-00261-2. eCollection 2021 Dec.
5
Involvement of Cholinergic, Adrenergic, and Glutamatergic Network Modulation with Cognitive Dysfunction in Alzheimer's Disease.胆碱能、肾上腺素能和谷氨酸能网络调节与阿尔茨海默病认知功能障碍的关系。
Int J Mol Sci. 2021 Feb 25;22(5):2283. doi: 10.3390/ijms22052283.
6
Excitatory Amino Acid Transporters in Physiology and Disorders of the Central Nervous System.兴奋性氨基酸转运体在中枢神经系统生理和疾病中的作用。
Int J Mol Sci. 2019 Nov 12;20(22):5671. doi: 10.3390/ijms20225671.
7
Hippocampal plasticity during the progression of Alzheimer's disease.阿尔茨海默病进展过程中的海马可塑性。
Neuroscience. 2015 Nov 19;309:51-67. doi: 10.1016/j.neuroscience.2015.03.006. Epub 2015 Mar 12.
8
Preferential accumulation of amyloid-beta in presynaptic glutamatergic terminals (VGluT1 and VGluT2) in Alzheimer's disease cortex.阿尔茨海默病皮质中淀粉样β优先积聚在突触前谷氨酸能末梢(VGluT1 和 VGluT2)。
Neurobiol Dis. 2012 Jan;45(1):381-7. doi: 10.1016/j.nbd.2011.08.027. Epub 2011 Sep 3.
9
Paradoxical upregulation of glutamatergic presynaptic boutons during mild cognitive impairment.轻度认知障碍期间谷氨酸能突触前终扣的反常上调
J Neurosci. 2007 Oct 3;27(40):10810-7. doi: 10.1523/JNEUROSCI.3269-07.2007.
10
Differential alterations of cortical glutamatergic binding sites in senile dementia of the Alzheimer type.阿尔茨海默型老年痴呆症中皮质谷氨酸能结合位点的差异性改变。
Proc Natl Acad Sci U S A. 1990 Feb;87(4):1352-6. doi: 10.1073/pnas.87.4.1352.