Sub-chronic aluminum exposure inhibits synaptic plasticity in hippocampus of rats via inhibiting PI3K/AKT/mTOR signaling pathway
10.11763/j.issn.2095-2619.2020.02.004
- Author:
Xingli XUE
1
;
Huan LI
1
;
Yaqin LI
1
;
Liang LI
1
;
Baolong PAN
1
;
Yanxia HAO
1
;
Qiao NIU
1
Author Information
1. School of Public Health, Shanxi Medical University Taiyuan, Shanxi 030001, China
- Publication Type:Journal Article
- Keywords:
Aluminum;
Learning and memory;
Synaptic plasticity;
Long-term potentiation;
Phosphatidylinositol 3 kinase;
Protein kinase B;
Rapamycin target protein;
Rat
- From:
China Occupational Medicine
2020;47(02):141-146
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE: To study the effect of sub-chronic aluminum exposure on synaptic plasticity in the hippocampus of rats and to explore the mechanism of phosphatidylinositol 3 kinase(PI3 K)/protein kinase B(AKT)/rapamycin target protein(mTOR) signaling pathway. METHODS: Specific pathogen free adult healthy male SD rats were randomly divided into control group and low-, medium-and high-dose groups based on body weight, with 10 rats in each group. Rats were treated with maltol aluminum solution at the concentrations of 0, 10, 20 and 40 μmol/kg body weight by intraperitoneal injection, 5 days per week for 3 months. After the exposure, rats were weighed. Morris water maze was used to test the learning and memory ability, and the two-electrode binding technique was used to record the long-term potentiation(LTP) amplitude in the hippocampus CA1 area of rats. The protein expression of PI3 K, AKT and mTOR in rat hippocampus tissues was detected by Western blot. RESULTS: After the exposure, the body weights of rats in the medium-and high-dose groups were lower than that of the control group(P<0.05). The results of the positioning navigation experiment showed that the escape latencies of the rats in the medium-and high-dose groups were shorter than that in the control group during the 2 nd to 4 th days of the experiment(P<0.05). The results of space exploration experiments showed that there was no statistical difference on the target quadrant retention time and the number of crossing the platform among the 4 groups(P>0.05). At 1, 30, and 60 min after high-frequency stimulation, the LTP amplitudes in the hippocampus CA1 area of the aluminum-treated groups were lower than that of the control group at the same time point(P<0.05), and the LTP amplitudes of hippocampus CA1 area of rats decreased with the increase of maltol aluminum exposure dose(P<0.01). The relative expression of PI3 K, AKT and mTOR protein in the hippocampus tissues of the aluminum-treated groups was lower than that of the control group(P<0.05), and the relative expression of the above three proteins decreased with the increase of the maltol aluminum exposure dose(P <0.01). CONCLUSION: Sub-chronic aluminum exposure could lead to dose-dependent inhibition of hippocampus synaptic plasticity in rats, thereby impairing the spatial learning ability of rats. This process may be related to inhibition of PI3 K/AKT/mTOR signaling pathway by aluminum.
