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. 2015 Mar 27;7(2):1759091415578714. doi: 10.1177/1759091415578714

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© The Author(s) 2015

This article is distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (http://www.uk.sagepub.com/aboutus/openaccess.htm).

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Figure 4. — Pharmacological characterization of ET-1 and BK activated SOCE in rat TG neurons. (a) Summary of changes in single-cell intracellular Ca²⁺ concentration as a measurement of SOCE induced by administration of ET-1 or BK in the presence or absence of various ion channel inhibitors: PyR3 (10 µM, TRPC3), Gd³⁺ (10 µM, ORAI), or combination of both. (b) Data from panel (a) as represented by percentage of maximal response inhibited by PyR3, Gd³⁺, or combination of both. (c) Summary of Orai1 ion channel contribution to ET-1- and BK-induced SOCE in rat TG neurons (single-cell measurements). (d) Summary of TRPC3 ion channel contribution to ET-1- and BK-induced SOCE in rat TG neurons (single-cell measurements). Statistical significance was assessed by two-way ANOVA with Bonferroni correction, n = 6–9, *p < .05. **p < .01. ***p < .001. ET-1 = endothelin-1; BK = bradykinin; SOCE = store-operated Ca²⁺ entry; TG = trigeminal ganglia; TRPC3 = transient receptor potential canonical channel 3; ORAI = ▪ ▪ ▪; ANOVA = analysis of variance.