Abstract |
Aluminum is a widespread environmental neurotoxicant that can induce Alzheimer's disease (AD)-like damage, such as neuronal injury and impairment of learning and memory. Several studies have shown that aluminum could reduce the synaptic plasticity, but its molecular mechanism remains unclear. In this study, rats were treated with aluminum maltol (Al(mal)3) to establish a toxic animal model and PMA was used to interfere with the expression of PKC. The Morris water maze and open field test were used to investigate the behavioral changes of the rats. Western blotting and RT-PCR were used to detect the expression levels of NMDAR subunits, PKC and CaMKII. The results showed that Al(mal)3 damaged learning and memory function and reduced anxiety in rats. During this process, the expression of PKC was downregulated and it inhibited the expression of NMDARs through the phosphorylation of CaMKII.
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Authors | Chanting He, Jingjing Ji, Xiaoyan Zhao, Yang Lei, Huan Li, Yanxia Hao, Shuhui Zhang, Jingsi Zhang, Chengjuan Liu, Jisheng Nie, Qiao Niu |
Journal | Neurotoxicity research
(Neurotox Res)
Vol. 39
Issue 6
Pg. 2042-2055
(Dec 2021)
ISSN: 1476-3524 [Electronic] United States |
PMID | 34499332
(Publication Type: Journal Article)
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Copyright | © 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. |
Chemical References |
- Receptors, N-Methyl-D-Aspartate
- Aluminum
- Protein Kinase C
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Topics |
- Aluminum
(toxicity)
- Animals
- Blotting, Western
- Dose-Response Relationship, Drug
- Hippocampus
(drug effects, metabolism)
- Learning
(drug effects)
- Male
- Memory
(drug effects)
- Morris Water Maze Test
(drug effects)
- Open Field Test
(drug effects)
- Protein Kinase C
(metabolism, physiology)
- Rats
- Rats, Sprague-Dawley
- Real-Time Polymerase Chain Reaction
- Receptors, N-Methyl-D-Aspartate
(metabolism, physiology)
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