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. 2017 Jun 14;7:3515. doi: 10.1038/s41598-017-03747-0

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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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Fluoxetine inhibits the ER calcium release and SOCE activation. (A) Fluoxetine inhibits thapsigargin-induced SOCE activation. Mean traces of [Ca²⁺]_i measurement from at least 70 different cells in each experiment. The SOCE amplitude indicates the rise of [Ca²⁺]_i in replenishment of [Ca²⁺]₀ from 0 to 2 mM. Arrow, adding 2 μM thapsigargin (Tg). (B) Quantitative analyses of Δ[Ca²⁺]_i. Each value represents mean ± SEM of at least 70 individual cells. ***P < 0.001 (C) Representative measurements of ER Ca²⁺ level ([Ca²⁺]_ER) in MIN6 cells. Mean traces of [Ca²⁺]_ER measurement from at least 30 different cells in each experiment. (D) Quantitative analyses of Δ[Ca²⁺]_ER. Each value represents mean ± SEM of at least 60 cells. *P < 0.05 (E) Fluoxetine blocks STIM1 membrane trafficking. Representative confocal images of endogenous STIM1 or transiently expressed eGFP-STIM1 at control and after 5 min of exposure to thapsigargin (2 μM) in MIN6 cells treated with or without fluoxetine. Scale bar, 5 μm.