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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 1. — Na⁺/K⁺-ATPase α2 deficiency increases SD susceptibility in acute brain slices. (a–b) SD speed and invaded area were imaged using light transmission changes (IOS). In the interface-type recording chamber, SD is characterized by a short increase (blue), followed by a long-lasting decrease of the IOS (red). Elevated baseline [K⁺]_o induced SD in the neocortex (nc) and frequently in the hippocampus (hipp) but not in the brainstem. (c) Stepwise increased baseline [K⁺]_o allowed for threshold assessment using ISMEs. (d) SD occurred at lower [K⁺]_ACSF in α2^+/KOE4 compared to WT. Co-application of 5 µM ouabain did not significantly add to the α2 deficiency effect on threshold [K⁺]_ACSF indicating ouabain action via the astrocytic and not the neuronal isoform. (e) SD latency was shorter in α2^+/KOE4 compared to WT mice confirming the lower [K⁺]_o threshold in α2-deficient mice. (f–g) Genetic α2 reduction did not affect [K⁺]_o peak and [K⁺]_o undershoot following SD. (h–i) Only pharmacological inhibition of the α2/3 portion of the Na⁺/K⁺-ATPase prolonged SD duration and decreased the DC amplitude irrespective of the genetic background. (j) SD speed was high under elevated [K⁺]_ACSF without additional effects of genetic or pharmacological α2 reduction. (k) IOS amplitude was not affected significantly by genetic or pharmacological α2 reduction. Sample sizes: α2^+/KOE4, n = 16–19; α2^+/+, n = 21–23. *p < 0.05.