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. 2018 Apr 12;9:362. doi: 10.3389/fphar.2018.00362

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Copyright © 2018 Chen, Wang, Zhang, Zhang, Chen, Zhao and Chen.

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 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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Acute treatment of SV enhances the trafficking of α7nAChR. (A,B) Representative Western blots of cell membrane surface (surface) and cytoplasmic α7nAChR protein in hippocampus. Biotin/beads: biotinylated samples. Graphs indicate the mean levels of surface α7nAChR (A) and cytoplasmic α7nAChR (B) in control and SV-treated hippocampus. Surface α7nAChR was normalized by surface GluR2 protein and cytoplasmic α7nAChR was normalized by β-actin, which was again normalized by vehicle-treated group. ^∗p < 0.05 and ^∗∗p < 0.01 vs. control slices (two-way ANOVA). (C) “Beads alone” indicates non-biotinylated samples as a negative control. (D) Total α7nAChR protein was normalized by β-actin, which was again normalized by vehicle-treated group.