| Literature DB >> 34499332 |
Chanting He1,2,3,4, Jingjing Ji5, Xiaoyan Zhao1, Yang Lei1, Huan Li1, Yanxia Hao1, Shuhui Zhang1, Jingsi Zhang1, Chengjuan Liu1, Jisheng Nie6,7,8, Qiao Niu9,10,11.
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.Entities:
Keywords: Aluminum; CaMKII; Learning and memory; N-methyl-D-aspartate receptor; Protein kinase C
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Year: 2021 PMID: 34499332 DOI: 10.1007/s12640-021-00407-0
Source DB: PubMed Journal: Neurotox Res ISSN: 1029-8428 Impact factor: 3.911