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. 2020 May 8;10:7815. doi: 10.1038/s41598-020-64783-x

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© The Author(s) 2020

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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Time course images of axonal damage and repair following midline fluid percussion injury (mFPI) and minocycline treatment. (A–F) Sham-vehicle mice have uniform axon morphology over the course of 30 days. In the injured groups, TBI-vehicle (G–L), TBI-45-min minocycline treated (M–R), and TBI-72-hr minocycline treated (S–X) mice all exhibit hallmarks of diffuse axonal injury (DAI) including varicosities (>), terminal bulbs (asterisks), and disappearing axons (dashed arrow). These hallmarks were quantified over the course of 30 days to demonstrate the effect of treatment on secondary axonal damage and repair. For each mouse, axons forming distinctive patterns in baseline images were used as landmarks. These axons were followed in each mouse throughout the time series to ensure that the same group of axons were imaged over time. One such axon is identified by a solid arrow in each panel. Images are z-stack projections (5 planes, 1 µm apart) of the same field of axons over time. Scale bars are 10 µm.