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Altered expression of myelin-associated inhibitors and their receptors after traumatic brain injury in the mouse
Uppsala University, Uppsala, Sweden.
Uppsala University, Uppsala, Sweden .
Uppsala University, Uppsala, Sweden .
Uppsala University, Uppsala, Sweden .
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2014 (English)In: Restorative Neurology and Neuroscience, ISSN 0922-6028, E-ISSN 1878-3627, Vol. 32, no 5, 717-731 p.Article in journal (Refereed) Published
Abstract [en]

Purpose: When central nervous system axons are injured, regeneration is partly inhibited by myelin-associated inhibitors (MAIs). Following traumatic brain injury (TBI) in the rat, pharmacological neutralisation of the MAIs Nogo-A and myelin-associated glycoprotein (MAG) resulted in improved functional outcome. In contrast, genetic or pharmacological neutralization of the MAI receptors Nogo-66receptor 1 (NgR1) or paired-immunoglobulin like receptor-B (PirB) showed an unaltered or impaired outcome following TBI in mice. The aim of the present study was thus to evaluate the MAI expressionlevels following TBI in mice. Methods: Quantitative reverse transcriptase PCR (qRT-PCR) was used to measure total RNA isolated from brains of young adult male C57BL/6 mice at one, three or seven days following controlled cortical impact TBI or sham injury. Hippocampal and neocortical tissue ipsi- and contralateral to the injury was analyzed for Nogo-A, oligodendrocyte-myelin glycoprotein (OMgp), MAG, and the MAI receptors PirB and NgR1, including its co-receptor Lingo1. Results: Compared to sham-injured controls, PirB neocortical expression was significantly upregulated at one day and NgR1expression downregulated at seven days post-TBI. In the hippocampus, transcriptional upregulation was observed in Nogo-A (one day post-injury), MAG and PirB at seven days post-injury. In contrast, the hippocampal transcripts of NgR1 and Lingo1 were decreased at seven days post-injury. The expression of OMgp was unaltered at all time points post-injury. Conclusion: These results suggest that early dynamic changes in MAI gene expression occur following TBI in the mouse, particularly in the hippocampus, which may play an inhibitory role for post-injury regeneration and plasticity.

Place, publisher, year, edition, pages
2014. Vol. 32, no 5, 717-731 p.
National Category
Engineering and Technology
Identifiers
URN: urn:nbn:se:mdh:diva-29683DOI: 10.3233/RNN-140419.Scopus ID: 2-s2.0-84907816087OAI: oai:DiVA.org:mdh-29683DiVA: diva2:875054
Available from: 2015-11-30 Created: 2015-11-26 Last updated: 2017-12-01Bibliographically approved

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