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. 2022 Jul 13;8:318. doi: 10.1038/s41420-022-01089-z

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© The Author(s) 2022

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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Fig. 6 — A On top of the figure are included representative rostral-caudal brain sections stained with cresyl violet of preconditioned hypoxic-ischemic (wild-type) and preconditioned hypoxic-ischemic (ncx3−/−) mice. Brain damage induced in mice was evaluated as % of ischemic damage at P11. Data are expressed as mean ± SD (n = 5–7). *P < 0.05 versus preconditioned hypoxic-ischemic (wild-type) mice. P-values were obtained by using Unpaired t-test. B, C The graphs show the time course of cliff avoidance and negative geotaxis reflex performances into two experimental groups: preconditioned hypoxic-ischemic (wild-type) and preconditioned hypoxic-ischemic (ncx3−/−) mice. Mice were monitored at different time intervals. Data are expressed as mean ± SD (n = 7–8). *P < 0.05 versus PC + HI mice (wild-type). P-values were obtained by using Unpaired t-test.