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. 2019 Dec 17;13:1351. doi: 10.3389/fnins.2019.01351

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Copyright © 2019 Ding, Gao, Gao, Meng, Zheng, Dong, Luo, Zhang, Shi and Rong.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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E2 and G-1 stimulate phosphorylation of MOR in a PKC-dependent manner. (A,B) SH-SY5Y cells treated with PMA (1 μM), E2 (1 μM), or G-1 (1 μM) for 30 min showed increased level of phosphorylated MOR (pMOR) as compared with the vehicle group. In the presence of the pan-PKC inhibitor (Ro 31-8820, Ro, 3 μM), E2 and G-1 failed to increase pMOR expression. (C) The averaged pMOR level (relative to β-actin) in cells with different treatments. After detection of pMOR (A,B), the nitrocellulose membrane was stripped and re-blocked by 5% fat-free dry milk in TBST, followed by incubation with MOR primary antibody, then MOR band was detected. ^∗∗P < 0.01, ^∗∗∗P < 0.001, one-way ANOVA with Tukey’s post hoc test, averaged data from three to four independent experiments.