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铜抑制小鼠海马切片中不依赖N-甲基-D-天冬氨酸受体的长时程增强，并在长时程增强后调节双脉冲比率。

Copper Inhibits NMDA Receptor-Independent LTP and Modulates the Paired-Pulse Ratio after LTP in Mouse Hippocampal Slices.

作者信息

Salazar-Weber Nina L, Smith Jeffrey P

机构信息

Department of Biology, Colorado State University-Pueblo, 2200 Bonforte Boulevard, Pueblo, CO 81001, USA.

出版信息

Int J Alzheimers Dis. 2011;2011:864753. doi: 10.4061/2011/864753. Epub 2011 Oct 19.

DOI:10.4061/2011/864753
PMID:22028985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3199118/
Abstract

Copper misregulation has been implicated in the pathological processes underlying deterioration of learning and memory in Alzheimer's disease and other neurodegenerative disorders. Supporting this, inhibition of long-term potentiation (LTP) by copper (II) has been well established, but the exact mechanism is poorly characterized. It is thought that an interaction between copper and postsynaptic NMDA receptors is a major part of the mechanism; however, in this study, we found that copper (II) inhibited NMDA receptor-independent LTP in the CA3 region of hippocampal slices. In addition, in the CA3 and CA1 regions, copper modulated the paired-pulse ratio (PPR) in an LTP-dependent manner. Combined, this suggests the involvement of a presynaptic mechanism in the modulation of synaptic plasticity by copper. Inhibition of the copper-dependent changes in the PPR with cyclothiazide suggested that this may involve an interaction with the presynaptic AMPA receptors that regulate neurotransmitter release.

摘要

铜代谢失调与阿尔茨海默病及其他神经退行性疾病中学习和记忆衰退的病理过程有关。与此相符的是，铜（II）对长时程增强（LTP）的抑制作用已得到充分证实，但其确切机制尚不清楚。人们认为铜与突触后NMDA受体之间的相互作用是该机制的主要部分；然而，在本研究中，我们发现铜（II）抑制海马切片CA3区中不依赖NMDA受体的LTP。此外，在CA3区和CA1区，铜以LTP依赖的方式调节配对脉冲比率（PPR）。综合来看，这表明铜在调节突触可塑性过程中涉及一种突触前机制。用环噻嗪抑制PPR中依赖铜的变化表明，这可能涉及与调节神经递质释放的突触前AMPA受体的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/8f793c1b1baa/IJAD2011-864753.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/348eeb25f909/IJAD2011-864753.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/242a1c58b17e/IJAD2011-864753.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/12f232aedc07/IJAD2011-864753.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/929cfcbdffec/IJAD2011-864753.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/0b6012decb66/IJAD2011-864753.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/9aa5077b8d4d/IJAD2011-864753.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/8f793c1b1baa/IJAD2011-864753.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/348eeb25f909/IJAD2011-864753.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/242a1c58b17e/IJAD2011-864753.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/12f232aedc07/IJAD2011-864753.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/929cfcbdffec/IJAD2011-864753.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/0b6012decb66/IJAD2011-864753.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/9aa5077b8d4d/IJAD2011-864753.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccef/3199118/8f793c1b1baa/IJAD2011-864753.007.jpg

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1
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Metallomics. 2011 Jul;3(7):726-34. doi: 10.1039/c1mt00015b. Epub 2011 Mar 28.
2
Zinc enhances long-term potentiation through P2X receptor modulation in the hippocampal CA1 region.锌通过调节海马 CA1 区 P2X 受体增强长时程增强。
Eur J Neurosci. 2011 Apr;33(7):1175-1185. doi: 10.1111/j.1460-9568.2010.07589.x. Epub 2011 Feb 17.
3
Copper handling machinery of the brain.脑内铜转运机制。
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Int J Mol Sci. 2023 Apr 6;24(7):6867. doi: 10.3390/ijms24076867.
4
Alternative Pharmacological Strategies for the Treatment of Alzheimer's Disease: Focus on Neuromodulator Function.治疗阿尔茨海默病的替代药理学策略：聚焦神经调节剂功能
Biomedicines. 2022 Nov 28;10(12):3064. doi: 10.3390/biomedicines10123064.
5
MST1-knockdown protects against impairment of working memory via regulating neural activity in depression-like mice.MST1 敲低通过调节抑郁样小鼠的神经活动保护工作记忆损伤。
Genes Brain Behav. 2022 Feb;21(2):e12782. doi: 10.1111/gbb.12782. Epub 2022 Jan 19.
6
Chronic Cyanuric Acid Exposure Depresses Hippocampal LTP but Does Not Disrupt Spatial Learning or Memory in the Morris Water Maze.慢性三聚氰胺暴露会抑制海马长时程增强，但不会破坏 Morris 水迷宫中的空间学习或记忆。
Neurotox Res. 2021 Aug;39(4):1148-1159. doi: 10.1007/s12640-021-00355-9. Epub 2021 Mar 22.
7
General Aspects of Metal Ions as Signaling Agents in Health and Disease.金属离子作为信号剂在健康和疾病中的一般作用。
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Metallomics. 2010 Sep;2(9):596-608. doi: 10.1039/c0mt00006j. Epub 2010 Aug 17.
4
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5
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6
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8
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9
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Neurobiol Aging. 2011 Feb;32(2):235-48. doi: 10.1016/j.neurobiolaging.2009.02.018. Epub 2009 Mar 25.
10
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