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. 2017 Jul 4;7:4583. doi: 10.1038/s41598-017-03041-z

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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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Effect of mutation on voltage-dependence of slow inactivation of Kv1.1 channels and on window currents. Cells were depolarized to various pre-pulse potentials, from −80 mV to +20 mV in +10 mV increments for 20 seconds, and then held at +40 mV test potential for 200 msec. Peak current amplitudes recorded at test potential of +40 mV were normalized (I/Imax) and these values were plotted as a function of the pre-pulse potentials and fitted with a Boltzmann function. The mutation resulted in the positive shift of the inactivation-voltage relationships for both homomeric (a) and heteromeric (b) channels. F303V reduced both (c) Kv1.1 and (d) Kv1.1/1.2 window currents (the triangular areas under the overlapping point of the activation and inactivation curves of the respective channel).