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. 2017 Sep 25;7:12245. doi: 10.1038/s41598-017-12561-7

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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The effect of TRPV4 antagonist and SK channel blocker on the outward currents and membrane potentials in PDGFRα⁺ cells. In cells dialyzed with K⁺-rich solutions, GSK (100 nM) activated outward current at a holding potential of −40 mV in voltage clamp mode. In the same cell, GSK induced hyperpolarization under current clamp (I = 0). TRPV4 antagonist, HC-067047 (1 μM, HC, a) and RN-1734 (10 μM, RN, c) inhibited GSK-activated outward current and hyperpolarization. Expanded time scales (b,d) from panels a and c during ramp depolarization before (a) and after (b) GSK application, respectively. In next experiments, cells were dialyzed with K⁺-rich solutions and held at −40 mV. GSK (100 nM) activated outward current. Addition of an SK channel blocker, UCL1684 (UCL, 1 μM) inhibited the outward currents and revealed an inward current. TRPV4 antagonist, HC-067047 (1 μM, HC) inhibited the inward current activated by GSK (e). Expanded time scales (f) from panel e during ramp depolarization (see inset) before (a), after (b) GSK and additional application of HC (c). Under pretreatment of UCL, GSK activated only inward current at a holding potential of −40 mV. Addition of HC completely blocked the inward current (g). Expanded time scales (h) from panel g during ramp depolarization before (a) and after (b) GSK application in the presence of UCL. PDGFRα⁺ cells from Trpv4 ^−/− mice were dialyzed with K⁺-rich solutions (i). GSK (100 nM) did not activate outward current at a holding potential of −40 mV. In the same cell, an SK channel activator (SKA-31, 10 µM) activated outward currents (i). Expanded time scales (j) from panel i during ramp depolarization in control (a), and before (b) and after (c) SKA-31 application, respectively.