Cargando…
Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury
Blast induced traumatic brain injury (B-TBI) may cause various degrees of cognitive and behavioral disturbances but the exact brain pathophysiology involved is poorly understood. It was previously suggested that ganglioside alteration on the axon surface as well as axonal regenerating inhibitors (AR...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5255550/ https://www.ncbi.nlm.nih.gov/pubmed/28112258 http://dx.doi.org/10.1038/srep41269 |
_version_ | 1782498556119089152 |
---|---|
author | Rubovitch, Vardit Zilberstein, Yael Chapman, Joab Schreiber, Shaul Pick, Chaim G. |
author_facet | Rubovitch, Vardit Zilberstein, Yael Chapman, Joab Schreiber, Shaul Pick, Chaim G. |
author_sort | Rubovitch, Vardit |
collection | PubMed |
description | Blast induced traumatic brain injury (B-TBI) may cause various degrees of cognitive and behavioral disturbances but the exact brain pathophysiology involved is poorly understood. It was previously suggested that ganglioside alteration on the axon surface as well as axonal regenerating inhibitors (ARIs) such as myelin associated glycoprotein (MAG) were involved in axonal outgrowth inhibition (AOI), leading to brain damage. GM1 ganglioside content in the brain was significantly reduced while GD1 ganglioside was not affected. The axonal regeneration was also reduced as seen by the phosphorylated NF-H expression. Moreover, B-TBI induced a significant elevation in MAG expression in the brains of the injured mice. The blast injured mice exhibited a significant decline in spatial memory as seen by the Y-maze test. In addition, the injured mice showed pronounced damage to the visual memory (as evaluated by the Novel object recognition test). A single low dose of GM1 (2 mg/kg; IP), shortly after the injury, prevented both the cognitive and the cellular changes in the brains of the injured mice. These results enlighten part of the complicated mechanism that underlies the damage induced by B-TBI and may also suggest a potential new treatment strategy for brain injuries. |
format | Online Article Text |
id | pubmed-5255550 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-52555502017-01-24 Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury Rubovitch, Vardit Zilberstein, Yael Chapman, Joab Schreiber, Shaul Pick, Chaim G. Sci Rep Article Blast induced traumatic brain injury (B-TBI) may cause various degrees of cognitive and behavioral disturbances but the exact brain pathophysiology involved is poorly understood. It was previously suggested that ganglioside alteration on the axon surface as well as axonal regenerating inhibitors (ARIs) such as myelin associated glycoprotein (MAG) were involved in axonal outgrowth inhibition (AOI), leading to brain damage. GM1 ganglioside content in the brain was significantly reduced while GD1 ganglioside was not affected. The axonal regeneration was also reduced as seen by the phosphorylated NF-H expression. Moreover, B-TBI induced a significant elevation in MAG expression in the brains of the injured mice. The blast injured mice exhibited a significant decline in spatial memory as seen by the Y-maze test. In addition, the injured mice showed pronounced damage to the visual memory (as evaluated by the Novel object recognition test). A single low dose of GM1 (2 mg/kg; IP), shortly after the injury, prevented both the cognitive and the cellular changes in the brains of the injured mice. These results enlighten part of the complicated mechanism that underlies the damage induced by B-TBI and may also suggest a potential new treatment strategy for brain injuries. Nature Publishing Group 2017-01-23 /pmc/articles/PMC5255550/ /pubmed/28112258 http://dx.doi.org/10.1038/srep41269 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Rubovitch, Vardit Zilberstein, Yael Chapman, Joab Schreiber, Shaul Pick, Chaim G. Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury |
title | Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury |
title_full | Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury |
title_fullStr | Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury |
title_full_unstemmed | Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury |
title_short | Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury |
title_sort | restoring gm1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5255550/ https://www.ncbi.nlm.nih.gov/pubmed/28112258 http://dx.doi.org/10.1038/srep41269 |
work_keys_str_mv | AT rubovitchvardit restoringgm1gangliosideexpressionamelioratesaxonaloutgrowthinhibitionandcognitiveimpairmentsinducedbyblasttraumaticbraininjury AT zilbersteinyael restoringgm1gangliosideexpressionamelioratesaxonaloutgrowthinhibitionandcognitiveimpairmentsinducedbyblasttraumaticbraininjury AT chapmanjoab restoringgm1gangliosideexpressionamelioratesaxonaloutgrowthinhibitionandcognitiveimpairmentsinducedbyblasttraumaticbraininjury AT schreibershaul restoringgm1gangliosideexpressionamelioratesaxonaloutgrowthinhibitionandcognitiveimpairmentsinducedbyblasttraumaticbraininjury AT pickchaimg restoringgm1gangliosideexpressionamelioratesaxonaloutgrowthinhibitionandcognitiveimpairmentsinducedbyblasttraumaticbraininjury |