莫里斯水上航行任务
突触可塑性
污渍
记忆障碍
开阔地
海马体
神经科学
NMDA受体
p38丝裂原活化蛋白激酶
蛋白激酶C
神经化学
磷酸化
化学
细胞生物学
生物
神经学
受体
内分泌学
蛋白激酶A
生物化学
认知
基因
作者
Chanting He,Jingjing Ji,Xiaoyan Zhao,Lei Yang,Huan Li,Yanxia Hao,Shuhui Zhang,Jingsi Zhang,Chengjuan Liu,Jisheng Nie,Qiao Niu
标识
DOI:10.1007/s12640-021-00407-0
摘要
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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