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. 2021 Oct 22;11:20886. doi: 10.1038/s41598-021-00389-1

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© The Author(s) 2021

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 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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Electrodiagnostic studies to measure latency and amplitude (a) (Sham, sham-operated mice; PBS, untreated mice during compression phase; CF, mice treated with clemastine during compression phase; d-PBS, untreated mice after surgical decompression; d-CF, mice treated with clemastine after surgical decompression). Serial measurements of latency and CMAP amplitude during 6 weeks of compression phase in mice with compression neuropathy (b,c) and during 2 weeks of decompression phase in mice taken surgical decompression (d,e). Error bars represent standard error of mean. Two-way ANOVA with Turkey’s post-hoc test was conducted. A significant difference (*p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001) versus PBS (control) or d-PBS group (n = 10 animals/group).