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. 2017 Apr 20;10:105. doi: 10.3389/fnmol.2017.00105

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Copyright © 2017 Yang, Zhou, Qian, Wang, He, Tang, Yin and Huang.

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) or licensor 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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Central administration of recombinant adropin mimicked anti-dipsogenic effects by activating TRPV4 neurons under normoxic condition in SFO. (A) The experimental design to study the mechanism of central anti-dipsogenic effects (Figures 3, 4). (B) TRPV4 (green) and c-Fos (red) within the same cells in SFO of wild-type rats after water deprivation for 12 h. The right panel shows a magnified view illustrating the overlap between c-Fos and TRPV4 positive signals. Nuclei were counterstained with DAPI (blue). Scale bar, 30 μm. (C) Construction of pAAV-ZsGreen-ShRNA cloning vector for S. thermophiles. (D) TRPV4 (visualized as brown staining) was down-regulated in SFO 7 days after injection of Trpv4 shRNA into the third ventricle. Scrambled shRNA was used as a control. Scale bar, 200 μm. (E) TRPV4 in SFO was detected by western blot. (F) Relative protein expression was calculated (n = 6 for each group, *P < 0.05). (G) Central administration of recombinant adropin (3 nM) inhibited water intake after 1 h and the inhibitory action of adropin was blocked by TRPV4 shRNA after 4 h in overnight water-deprived rats (n = 8 for each group; *P < 0.05 vs. control group; ^#P < 0.05 vs. recombinant adropin group).