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. 2021 May 5;11:9616. doi: 10.1038/s41598-021-89032-7

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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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PTX3 depletion did not affect TBI outcome. (A, B) Sensorimotor function was assessed over 4 weeks after sham injury or TBI using Composite neuroscore (A, worst score = 0) and Beam walk (B, worst score = 60) tests in WT and PTX3 KO mice. (C, D) No difference was observed in post-traumatic sensorimotor deficits between the two strains. Data is presented as mean ± SEM, n = 5 (Sham/TBI WT), n = 10 (Sham PTX3 KO), n = 12 (TBI PTX3 KO). Two-way ANOVA for repeated measures followed by Bonferroni post hoc test = ns. Five weeks after TBI, neither the lesion volume (E) nor the neuronal density (F, neurons per mm²) in the lesioned cortex varied between WT and PTX3 KO mice. Data is presented as mean ± SEM, n = 5 (TBI WT/PTX3 KO). Unpaired t-test = ns (E).