Role of mGluR 1 in synaptic plasticity impairment induced by maltol aluminium in rats
Copyright © 2020. Published by Elsevier B.V..
The main symptoms of Alzheimer's disease (AD) is the loss of learning and memory ability, of which biological basis is synaptic plasticity. Aluminium has been found to cause changes in synaptic plasticity, but its molecular mechanism was unclear. In this study, Sprague-Dawley rats were injected with aluminium maltol (Al(mal)3) through the lateral ventricle to establish an AD-like model. Y-maze, electrophysiological measurements, Golgi staining, scanning electron microscopy, quantitative real-time polymerase chain reaction, and western blot techniques were used to investigate regulation of the metabolic glutamate receptor 1 (mGluR1) in synaptic plasticity impairment induced by Al(mal)3. The results showed that Al(mal)3 inhibited the induction and maintenance of long-term potentiation in the hippocampal CA1 region. During this process, the expression of mGluR1 was up-regulated and it inhibited the expression and phosphorylation of the N-methyl-D-aspartic acid receptors (NMDARs). This mainly affected NMDAR1 and NMDAR2B but did not affect protein kinase C expression.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2020 |
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| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:78 |
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| Enthalten in: |
Environmental toxicology and pharmacology - 78(2020) vom: 22. Aug., Seite 103406 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Pan, Baolong [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 04.01.2021 Date Revised 04.01.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.etap.2020.103406 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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NLM310205891 |
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| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2020. Published by Elsevier B.V. | ||
| 520 | |a The main symptoms of Alzheimer's disease (AD) is the loss of learning and memory ability, of which biological basis is synaptic plasticity. Aluminium has been found to cause changes in synaptic plasticity, but its molecular mechanism was unclear. In this study, Sprague-Dawley rats were injected with aluminium maltol (Al(mal)3) through the lateral ventricle to establish an AD-like model. Y-maze, electrophysiological measurements, Golgi staining, scanning electron microscopy, quantitative real-time polymerase chain reaction, and western blot techniques were used to investigate regulation of the metabolic glutamate receptor 1 (mGluR1) in synaptic plasticity impairment induced by Al(mal)3. The results showed that Al(mal)3 inhibited the induction and maintenance of long-term potentiation in the hippocampal CA1 region. During this process, the expression of mGluR1 was up-regulated and it inhibited the expression and phosphorylation of the N-methyl-D-aspartic acid receptors (NMDARs). This mainly affected NMDAR1 and NMDAR2B but did not affect protein kinase C expression | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Maltol aluminium | |
| 650 | 4 | |a Metabolic glutamate receptor 1 | |
| 650 | 4 | |a N-methyl-D-aspartic acid receptor | |
| 650 | 4 | |a Protein kinase C | |
| 650 | 4 | |a Synaptic plasticity impairment | |
| 650 | 7 | |a Organometallic Compounds |2 NLM | |
| 650 | 7 | |a Pyrones |2 NLM | |
| 650 | 7 | |a Receptors, Metabotropic Glutamate |2 NLM | |
| 650 | 7 | |a Receptors, N-Methyl-D-Aspartate |2 NLM | |
| 650 | 7 | |a metabotropic glutamate receptor type 1 |2 NLM | |
| 650 | 7 | |a aluminum maltolate |2 NLM | |
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| 700 | 1 | |a Zhang, Jingsi |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Yue |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Liang |e verfasserin |4 aut | |
| 700 | 1 | |a Xue, Xingli |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Huan |e verfasserin |4 aut | |
| 700 | 1 | |a Niu, Qiao |e verfasserin |4 aut | |
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