Aluminum-Induced Synaptic Plasticity Impairment via PI3K-Akt-mTOR Signaling Pathway

被引:45
|
作者
Li, Huan [1 ,2 ,3 ]
Xue, Xingli [1 ,2 ]
Li, Liang [1 ,2 ]
Li, Yaqin [1 ,2 ]
Wang, Yanni [1 ,2 ]
Huang, Tao [1 ,2 ]
Wang, Yanhong [1 ,2 ]
Meng, Huaxing [1 ]
Pan, Baolong [1 ]
Niu, Qiao [1 ,2 ,3 ]
机构
[1] Shanxi Med Univ, Sch Publ Hlth, Dept Occupat Hlth, Xinjian South Rd, Taiyuan, Shanxi, Peoples R China
[2] Shanxi Med Univ, Key Lab Environm Hazard & Hlth Shanxi Prov, Taiyuan, Peoples R China
[3] Shanxi Med Univ, Educ Minist, Key Lab Cellular Physiol, Taiyuan, Peoples R China
基金
中国国家自然科学基金;
关键词
Aluminum; Synaptic plasticity; Phosphatidylinositol 3-kinase (PI3K); Protein kinase B (Akt); Mammalian target of rapamycin (mTOR); LONG-TERM POTENTIATION; MORPHOLOGICAL-CHANGES; DENDRITE MORPHOLOGY; ALZHEIMERS-DISEASE; AMPA RECEPTORS; HIPPOCAMPUS; EXPOSURE; CORTEX; MEMORY; RATS;
D O I
10.1007/s12640-020-00165-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Aluminum (Al) is an environmental neurotoxin with extensive exposure by humans, but the molecular mechanism of its toxicity is still unclear. Several studies have indicated that exposure to aluminum can impair learning and memory function. The purpose of this study was to investigate the mechanism of LTP injury and the effect of aluminum exposure on related signal pathways. The results showed that the axonal dendrites of neurons in the hippocampal CA1 area of rats exposed to maltol aluminum showed neuritic beading and the dendritic spines were reduced. This resulted in dose-dependent LTP inhibition and led to impaired learning and memory function in rats. The PI3K-Akt-mTOR pathway may play a crucial role in this process.
引用
收藏
页码:996 / 1008
页数:13
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