Objective:To investigate the Alzheimer disease(AD)-like changes caused by methamphetamine(METH)exposure,and to elucidate the role of L-type calcium channels in this pathological change. Methods:After primary cultured neurons were exposed to METH(0,30,100,300,and 1 000 μmol/L),Western blotting assay was performed to investigate the expression of AD-like pathological protein amyloid precursor protein(APP)and p-Tau with or without the treatment of nifedipine. Results:After METH treatment,APP and p-Tau increased in a dose-dependent manner. Meanwhile,with a certain concentration of METH cultured with the neurons,the level of APP and p-Tau was increased in a time-dependent manner. After pre-incubation with the calcium channel inhibitor nifedipine(NIF),the METH-induced AD-like changes were significantly improved. Conclusion:METH exposure can cause AD pathological protein changes and L-type calcium channel ihhibitor can partially reverse the adverse changes,therefore,L-type calcium channel may be a potential intervention target for METH with the potential intervention value.
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Hu Xin, Lü Mengqian, Wang Yu, Jiang Lei, Wang Jun, Xia Zhengrong, Xia Lei. Involvement of the L⁃type Ca2 + channel in methamphetamine⁃induced APP and p⁃Tau upregulation[J].,2019,(4):491-494.