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. 2019 Feb 28;40(3):622–638. doi: 10.1177/0271678X19833757

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© The Author(s) 2019

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 2. — SD threshold reduction is specific to deficiency of the α2 isoform in acute brain slices. (a) Only α2 deficiency or pharmacological inhibition with 5 µM ouabain significantly reduced SD threshold [K⁺]_o, whereas α1 and α3 deficiency did not significantly affect threshold [K⁺]_o as measured by ISMEs. (b) SD latency: α2^+/KOE4 segregate from the high into the low threshold group together with ouabain, indicated by the significantly shorter time until SD occurrence (below the red dashed line). (c) Peak [K⁺]_o during SD was significantly lower in α1^+/KOE15 mice. (d) The duration of the accompanying DC shift was longer only under ouabain exposure, whereas α isoform deficiency had no effect. (e) The DC amplitude was reduced in α3^+/KOI4 and in presence of 5 µM ouabain. Sample sizes: α2^+/KOE4/α2^+/+, n = 17–23; α3^+/KOI4/ α3^+/+, n = 10–14; α1^+/KOE15/ α1^+/+, n = 6–8. *P < 0.05.