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Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain

BACKGROUND: Reports show that stressful events before injury exacerbates post-injury pain. The mechanism underlying stress-induced heightened thermal pain is unclear. Here, we examined the effects of chronic intermittent stress (CIS) on nociceptive behaviors and brain-derived nerve growth factor (BD...

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Autores principales: Sosanya, Natasha M., Garza, Thomas H., Stacey, Winfred, Crimmins, Stephen L., Christy, Robert J., Cheppudira, Bopaiah P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6480655/
https://www.ncbi.nlm.nih.gov/pubmed/31014242
http://dx.doi.org/10.1186/s12868-019-0500-1
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author Sosanya, Natasha M.
Garza, Thomas H.
Stacey, Winfred
Crimmins, Stephen L.
Christy, Robert J.
Cheppudira, Bopaiah P.
author_facet Sosanya, Natasha M.
Garza, Thomas H.
Stacey, Winfred
Crimmins, Stephen L.
Christy, Robert J.
Cheppudira, Bopaiah P.
author_sort Sosanya, Natasha M.
collection PubMed
description BACKGROUND: Reports show that stressful events before injury exacerbates post-injury pain. The mechanism underlying stress-induced heightened thermal pain is unclear. Here, we examined the effects of chronic intermittent stress (CIS) on nociceptive behaviors and brain-derived nerve growth factor (BDNF) system in the prefrontal cortex (PFC) and hypothalamus of rats with and without thermal injury. RESULTS: Unstressed rats showed transient mechanical allodynia during stress exposure. Stressed rats with thermal injury displayed persistent exacerbated mechanical allodynia (P < 0.001). Increased expression of BDNF mRNA in the PFC (P < 0.05), and elevated TrkB and p-TrkB (P < 0.05) protein levels in the hypothalamus were observed in stressed rats with thermal injury but not in stressed or thermally injured rats alone. Furthermore, administration of CTX-B significantly reduced stress-induced exacerbated mechanical allodynia in thermally injured rats (P < 0.001). CONCLUSION: These results indicate that BDNF-TrkB signaling in PFC and hypothalamus contributes to CIS-induced exacerbated mechanical allodynia in thermal injury state. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12868-019-0500-1) contains supplementary material, which is available to authorized users.
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spelling pubmed-64806552019-05-01 Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain Sosanya, Natasha M. Garza, Thomas H. Stacey, Winfred Crimmins, Stephen L. Christy, Robert J. Cheppudira, Bopaiah P. BMC Neurosci Research Article BACKGROUND: Reports show that stressful events before injury exacerbates post-injury pain. The mechanism underlying stress-induced heightened thermal pain is unclear. Here, we examined the effects of chronic intermittent stress (CIS) on nociceptive behaviors and brain-derived nerve growth factor (BDNF) system in the prefrontal cortex (PFC) and hypothalamus of rats with and without thermal injury. RESULTS: Unstressed rats showed transient mechanical allodynia during stress exposure. Stressed rats with thermal injury displayed persistent exacerbated mechanical allodynia (P < 0.001). Increased expression of BDNF mRNA in the PFC (P < 0.05), and elevated TrkB and p-TrkB (P < 0.05) protein levels in the hypothalamus were observed in stressed rats with thermal injury but not in stressed or thermally injured rats alone. Furthermore, administration of CTX-B significantly reduced stress-induced exacerbated mechanical allodynia in thermally injured rats (P < 0.001). CONCLUSION: These results indicate that BDNF-TrkB signaling in PFC and hypothalamus contributes to CIS-induced exacerbated mechanical allodynia in thermal injury state. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12868-019-0500-1) contains supplementary material, which is available to authorized users. BioMed Central 2019-04-24 /pmc/articles/PMC6480655/ /pubmed/31014242 http://dx.doi.org/10.1186/s12868-019-0500-1 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Sosanya, Natasha M.
Garza, Thomas H.
Stacey, Winfred
Crimmins, Stephen L.
Christy, Robert J.
Cheppudira, Bopaiah P.
Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain
title Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain
title_full Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain
title_fullStr Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain
title_full_unstemmed Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain
title_short Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain
title_sort involvement of brain-derived neurotrophic factor (bdnf) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6480655/
https://www.ncbi.nlm.nih.gov/pubmed/31014242
http://dx.doi.org/10.1186/s12868-019-0500-1
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