Abstract |
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.
|
Authors | Baolong Pan, Yaqin Li, Jingsi Zhang, Yue Zhou, Liang Li, Xingli Xue, Huan Li, Qiao Niu |
Journal | Environmental toxicology and pharmacology
(Environ Toxicol Pharmacol)
Vol. 78
Pg. 103406
(Aug 2020)
ISSN: 1872-7077 [Electronic] Netherlands |
PMID | 32438325
(Publication Type: Journal Article)
|
Copyright | Copyright © 2020. Published by Elsevier B.V. |
Chemical References |
- Organometallic Compounds
- Pyrones
- Receptors, Metabotropic Glutamate
- Receptors, N-Methyl-D-Aspartate
- metabotropic glutamate receptor type 1
- aluminum maltolate
- Protein Kinase C
|
Topics |
- Animals
- Hippocampus
(drug effects, physiology, ultrastructure)
- Male
- Microscopy, Electron, Transmission
- Neuronal Plasticity
(drug effects)
- Neurons
(drug effects, ultrastructure)
- Organometallic Compounds
(toxicity)
- Protein Kinase C
(metabolism)
- Pyrones
(toxicity)
- Rats, Sprague-Dawley
- Receptors, Metabotropic Glutamate
(physiology)
- Receptors, N-Methyl-D-Aspartate
(metabolism)
|