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. 2020 Feb 20;115(2):20. doi: 10.1007/s00395-020-0780-8

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Effects of Na_V1.8 on the murine atrial action potential using SCN10A^−/− and WT mice. Data are presented as mean ± SEM. P values were calculated using one-way ANOVA with Tukey's test for multiple comparisons. a Representative action potential recordings (1 Hz stimulation) of isolated murine atrial cardiomyocytes. b Effects of genetic ablation of Na_V1.8 (SCN10A^−/−: n = 16 cells/10 mice) compared to WT (n = 14 cells/8 mice) and effects of pharmacological inhibition of Na_V1.8 by PF-01247324 in each genotype (SCN10A^−/−: n = 15 cells/10 mice and WT: n = 13/8) on action potential (AP) amplitude, (c) maximum upstroke velocity (dv/dt), (d) resting membrane potential (RMP) and action potential duration at (e) 50% (APD₅₀) and (f) 90% repolarization (APD₉₀)