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Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression

Traumatic brain injury (TBI) affects over 69 million people annually worldwide, and those with pre-existing depression have worse recovery. The molecular mechanisms that may contribute to poor recovery after TBI with co-morbid depression have not been established. TBI and depression have many common...

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Autores principales: Knott, Maxon V., Ngwenya, Laura B., Correll, Erika A., Bohnert, Judy, Ziemba, Noah J., Allgire, Emily, Hopkins, Tracy, McGuire, Jennifer L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8347641/
https://www.ncbi.nlm.nih.gov/pubmed/34360865
http://dx.doi.org/10.3390/ijms22158086
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author Knott, Maxon V.
Ngwenya, Laura B.
Correll, Erika A.
Bohnert, Judy
Ziemba, Noah J.
Allgire, Emily
Hopkins, Tracy
McGuire, Jennifer L.
author_facet Knott, Maxon V.
Ngwenya, Laura B.
Correll, Erika A.
Bohnert, Judy
Ziemba, Noah J.
Allgire, Emily
Hopkins, Tracy
McGuire, Jennifer L.
author_sort Knott, Maxon V.
collection PubMed
description Traumatic brain injury (TBI) affects over 69 million people annually worldwide, and those with pre-existing depression have worse recovery. The molecular mechanisms that may contribute to poor recovery after TBI with co-morbid depression have not been established. TBI and depression have many commonalities including volume changes, myelin disruption, changes in proliferation, and changes in glutamatergic signaling. We used a well-established animal model of depression, the Wistar Kyoto (WKY) rat, to elucidate changes after TBI that may influence the recovery trajectory. We compared the histological and molecular outcomes in the hippocampal dentate gyrus after experimental TBI using the lateral fluid percussion injury (LFPI) in the WKY and the parent Wistar (WIS) strain. We showed that WKY had exaggerated myelin loss after LFPI and baseline deficits in proliferation. In addition, we showed that while after LFPI WIS rats exhibited glutamate receptor subunit changes, namely increased GluN2B, the WKY rats failed to show such injury-related changes. These differential responses to LFPI helped to elucidate the molecular characteristics that influence poor recovery after TBI in those with pre-existing depression and may lead to targets for future therapeutic interventions.
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spelling pubmed-83476412021-08-08 Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression Knott, Maxon V. Ngwenya, Laura B. Correll, Erika A. Bohnert, Judy Ziemba, Noah J. Allgire, Emily Hopkins, Tracy McGuire, Jennifer L. Int J Mol Sci Article Traumatic brain injury (TBI) affects over 69 million people annually worldwide, and those with pre-existing depression have worse recovery. The molecular mechanisms that may contribute to poor recovery after TBI with co-morbid depression have not been established. TBI and depression have many commonalities including volume changes, myelin disruption, changes in proliferation, and changes in glutamatergic signaling. We used a well-established animal model of depression, the Wistar Kyoto (WKY) rat, to elucidate changes after TBI that may influence the recovery trajectory. We compared the histological and molecular outcomes in the hippocampal dentate gyrus after experimental TBI using the lateral fluid percussion injury (LFPI) in the WKY and the parent Wistar (WIS) strain. We showed that WKY had exaggerated myelin loss after LFPI and baseline deficits in proliferation. In addition, we showed that while after LFPI WIS rats exhibited glutamate receptor subunit changes, namely increased GluN2B, the WKY rats failed to show such injury-related changes. These differential responses to LFPI helped to elucidate the molecular characteristics that influence poor recovery after TBI in those with pre-existing depression and may lead to targets for future therapeutic interventions. MDPI 2021-07-28 /pmc/articles/PMC8347641/ /pubmed/34360865 http://dx.doi.org/10.3390/ijms22158086 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Knott, Maxon V.
Ngwenya, Laura B.
Correll, Erika A.
Bohnert, Judy
Ziemba, Noah J.
Allgire, Emily
Hopkins, Tracy
McGuire, Jennifer L.
Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression
title Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression
title_full Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression
title_fullStr Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression
title_full_unstemmed Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression
title_short Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression
title_sort lack of glutamate receptor subunit expression changes in hippocampal dentate gyrus after experimental traumatic brain injury in a rodent model of depression
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8347641/
https://www.ncbi.nlm.nih.gov/pubmed/34360865
http://dx.doi.org/10.3390/ijms22158086
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