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Open AccessArticle

Diffuse Axonal Injury in the Rat Brain: Axonal Injury and Oligodendrocyte Activity Following Rotational Injury

1
Department of Neuroscience, Karolinska Institute, 171 77 Stockholm, Sweden
2
Department of Molecular Medicine, Università degli Studi di Pavia, 27100 Pavia, Italy
3
Department of Mechanics and Maritime Sciences, Chalmers University of Technology, 412 96 Gothenburg, Sweden
4
Department of Neuroscience, Section of Neurosurgery, Uppsala University, 751 85 Uppsala, Sweden
*
Author to whom correspondence should be addressed.
Brain Sci. 2020, 10(4), 229; https://doi.org/10.3390/brainsci10040229
Received: 6 February 2020 / Revised: 3 April 2020 / Accepted: 7 April 2020 / Published: 10 April 2020
(This article belongs to the Section Neuroglia)
Traumatic brain injury (TBI) commonly results in primary diffuse axonal injury (DAI) and associated secondary injuries that evolve through a cascade of pathological mechanisms. We aim at assessing how myelin and oligodendrocytes react to head angular-acceleration-induced TBI in a previously described model. This model induces axonal injuries visible by amyloid precursor protein (APP) expression, predominantly in the corpus callosum and its borders. Brain tissue from a total of 27 adult rats was collected at 24 h, 72 h and 7 d post-injury. Coronal sections were prepared for immunohistochemistry and RNAscope® to investigate DAI and myelin changes (APP, MBP, Rip), oligodendrocyte lineage cell loss (Olig2), oligodendrocyte progenitor cells (OPCs) (NG2, PDGFRa) and neuronal stress (HSP70, ATF3). Oligodendrocytes and OPCs numbers (expressed as percentage of positive cells out of total number of cells) were measured in areas with high APP expression. Results showed non-statistically significant trends with a decrease in oligodendrocyte lineage cells and an increase in OPCs. Levels of myelination were mostly unaltered, although Rip expression differed significantly between sham and injured animals in the frontal brain. Neuronal stress markers were induced at the dorsal cortex and habenular nuclei. We conclude that rotational injury induces DAI and neuronal stress in specific areas. We noticed indications of oligodendrocyte death and regeneration without statistically significant changes at the timepoints measured, despite indications of axonal injuries and neuronal stress. This might suggest that oligodendrocytes are robust enough to withstand this kind of trauma, knowledge important for the understanding of thresholds for cell injury and post-traumatic recovery potential. View Full-Text
Keywords: diffuse axonal injury; traumatic brain injury; myelin degradation; oligodendrocyte progenitor cell; olig2 diffuse axonal injury; traumatic brain injury; myelin degradation; oligodendrocyte progenitor cell; olig2
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Losurdo, M.; Davidsson, J.; Sköld, M.K. Diffuse Axonal Injury in the Rat Brain: Axonal Injury and Oligodendrocyte Activity Following Rotational Injury. Brain Sci. 2020, 10, 229.

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