Journal
NEUROTOXICITY RESEARCH
Volume 37, Issue 4, Pages 996-1008Publisher
SPRINGER
DOI: 10.1007/s12640-020-00165-5
Keywords
Aluminum; Synaptic plasticity; Phosphatidylinositol 3-kinase (PI3K); Protein kinase B (Akt); Mammalian target of rapamycin (mTOR)
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Funding
- National Natural Science Foundation of China [81872599, 81430078]
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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.
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