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...

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Autores principales: Shih, Hsi-Chien, Kuan, Yung-Hui, Shyu, Bai-Chung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer 2017
Materias:
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.
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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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