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Relevance of gap junctions and large pore channels in traumatic brain injury

In case of traumatic brain injury (TBI), occurrence of central nervous tissue damage is frequently aligned with local modulations of neuronal and glial gap junction channel expression levels. The degree of gap junctional protein expression and intercellular coupling efficiency, as well as hemichanne...

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Autor principal: Prochnow, Nora
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3920098/
https://www.ncbi.nlm.nih.gov/pubmed/24575046
http://dx.doi.org/10.3389/fphys.2014.00031
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author Prochnow, Nora
author_facet Prochnow, Nora
author_sort Prochnow, Nora
collection PubMed
description In case of traumatic brain injury (TBI), occurrence of central nervous tissue damage is frequently aligned with local modulations of neuronal and glial gap junction channel expression levels. The degree of gap junctional protein expression and intercellular coupling efficiency, as well as hemichannel function has substantially impact on the course of trauma recovery and outcome. During TBI, gap junctions are especially involved in the intercellular molecule trafficking on repair of blood vessels and the regulation of vasomotor tone. Furthermore, gliosis and astrocytic swelling due to mechanical strain injury point out the consequences of derailed gap junction communication. This review addresses the outstanding role of gap junction channels in TBI pathophysiology and links the current state of results to applied clinical procedures as well as perspectives in acute and long-term treatment options.
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spelling pubmed-39200982014-02-26 Relevance of gap junctions and large pore channels in traumatic brain injury Prochnow, Nora Front Physiol Physiology In case of traumatic brain injury (TBI), occurrence of central nervous tissue damage is frequently aligned with local modulations of neuronal and glial gap junction channel expression levels. The degree of gap junctional protein expression and intercellular coupling efficiency, as well as hemichannel function has substantially impact on the course of trauma recovery and outcome. During TBI, gap junctions are especially involved in the intercellular molecule trafficking on repair of blood vessels and the regulation of vasomotor tone. Furthermore, gliosis and astrocytic swelling due to mechanical strain injury point out the consequences of derailed gap junction communication. This review addresses the outstanding role of gap junction channels in TBI pathophysiology and links the current state of results to applied clinical procedures as well as perspectives in acute and long-term treatment options. Frontiers Media S.A. 2014-02-11 /pmc/articles/PMC3920098/ /pubmed/24575046 http://dx.doi.org/10.3389/fphys.2014.00031 Text en Copyright © 2014 Prochnow. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Prochnow, Nora
Relevance of gap junctions and large pore channels in traumatic brain injury
title Relevance of gap junctions and large pore channels in traumatic brain injury
title_full Relevance of gap junctions and large pore channels in traumatic brain injury
title_fullStr Relevance of gap junctions and large pore channels in traumatic brain injury
title_full_unstemmed Relevance of gap junctions and large pore channels in traumatic brain injury
title_short Relevance of gap junctions and large pore channels in traumatic brain injury
title_sort relevance of gap junctions and large pore channels in traumatic brain injury
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3920098/
https://www.ncbi.nlm.nih.gov/pubmed/24575046
http://dx.doi.org/10.3389/fphys.2014.00031
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