Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model
Approximately 7% to 10% of patients develop a chronic pain syndrome after stroke. This chronic pain condition is called central poststroke pain (CPSP). Recent studies have observed an abnormal increase in the secretion of brain-derived neurotrophic factor (BDNF) in spinal cord tissue after spinal co...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Wolters Kluwer
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5472007/ https://www.ncbi.nlm.nih.gov/pubmed/28394853 http://dx.doi.org/10.1097/j.pain.0000000000000915 |
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author | Shih, Hsi-Chien Kuan, Yung-Hui Shyu, Bai-Chung |
author_facet | Shih, Hsi-Chien Kuan, Yung-Hui Shyu, Bai-Chung |
author_sort | Shih, Hsi-Chien |
collection | PubMed |
description | Approximately 7% to 10% of patients develop a chronic pain syndrome after stroke. This chronic pain condition is called central poststroke pain (CPSP). Recent studies have observed an abnormal increase in the secretion of brain-derived neurotrophic factor (BDNF) in spinal cord tissue after spinal cord injury. An animal model of CPSP was established by an intrathalamus injection of collagenase. Mechanical and thermal allodynia was induced after lesions of the thalamic ventral basal complex in rats. Four weeks after the injection, the number of neurons decreased, the number of astrocytes, microglia, and P2X4 receptors increased, and BDNF mRNA expression increased in the brain lesion area. Nociceptive activity in the medial thalamus (MT) and the coherence coefficient of spontaneous field potential oscillations in the anterior cingulate cortex were enhanced in CPSP animals, and these enhancements were blocked by an acute injection of TrkB-Fc and TrkB antagonist Tat Cyclotraxin-B. Instead of being inhibited by the γ-aminobutyric acid (GABA) system in normal rats, multiunit activity in the MT was enhanced after a microinjection of muscimol, a GABA(A) receptor agonist, in CPSP animals. After CPSP, BDNF expression was enhanced in the MT, whereas the expression of GABA(A) channels and the cotransporter KCC2 decreased in the same area. These findings suggest that neuronal plasticity in the MT that was induced by BDNF overexpression after the thalamic lesion was a key factor in CPSP. |
format | Online Article Text |
id | pubmed-5472007 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Wolters Kluwer |
record_format | MEDLINE/PubMed |
spelling | pubmed-54720072017-06-30 Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model Shih, Hsi-Chien Kuan, Yung-Hui Shyu, Bai-Chung Pain Research Paper Approximately 7% to 10% of patients develop a chronic pain syndrome after stroke. This chronic pain condition is called central poststroke pain (CPSP). Recent studies have observed an abnormal increase in the secretion of brain-derived neurotrophic factor (BDNF) in spinal cord tissue after spinal cord injury. An animal model of CPSP was established by an intrathalamus injection of collagenase. Mechanical and thermal allodynia was induced after lesions of the thalamic ventral basal complex in rats. Four weeks after the injection, the number of neurons decreased, the number of astrocytes, microglia, and P2X4 receptors increased, and BDNF mRNA expression increased in the brain lesion area. Nociceptive activity in the medial thalamus (MT) and the coherence coefficient of spontaneous field potential oscillations in the anterior cingulate cortex were enhanced in CPSP animals, and these enhancements were blocked by an acute injection of TrkB-Fc and TrkB antagonist Tat Cyclotraxin-B. Instead of being inhibited by the γ-aminobutyric acid (GABA) system in normal rats, multiunit activity in the MT was enhanced after a microinjection of muscimol, a GABA(A) receptor agonist, in CPSP animals. After CPSP, BDNF expression was enhanced in the MT, whereas the expression of GABA(A) channels and the cotransporter KCC2 decreased in the same area. These findings suggest that neuronal plasticity in the MT that was induced by BDNF overexpression after the thalamic lesion was a key factor in CPSP. Wolters Kluwer 2017-04-05 2017-07 /pmc/articles/PMC5472007/ /pubmed/28394853 http://dx.doi.org/10.1097/j.pain.0000000000000915 Text en Copyright © 2017 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND) (http://creativecommons.org/licenses/by-nc-nd/4.0/) , where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. |
spellingShingle | Research Paper Shih, Hsi-Chien Kuan, Yung-Hui Shyu, Bai-Chung Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model |
title | Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model |
title_full | Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model |
title_fullStr | Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model |
title_full_unstemmed | Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model |
title_short | Targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model |
title_sort | targeting brain-derived neurotrophic factor in the medial thalamus for the treatment of central poststroke pain in a rodent model |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5472007/ https://www.ncbi.nlm.nih.gov/pubmed/28394853 http://dx.doi.org/10.1097/j.pain.0000000000000915 |
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