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A non-opioid pathway for dynorphin-caused spinal cord injury in rats☆

Intrathecal injection of dynorphin into rats via subarachnoid catheter induces damage to spinal cord tissue and motor function. Injection of the kappa opioid receptor antagonist nor-binaltorphine, or the excitatory amino acid N-methyl-D-aspartate receptor antagonist MK-801 into rats alleviated the p...

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Autores principales: Chen, Yu, Xiang, Liangbi, Liu, Jun, Zhou, Dapeng, Yu, Hailong, Wang, Qi, Han, Wenfeng, Guo, Mingming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4342707/
https://www.ncbi.nlm.nih.gov/pubmed/25737707
http://dx.doi.org/10.3969/j.issn.1673-5374.2012.11.003
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author Chen, Yu
Xiang, Liangbi
Liu, Jun
Zhou, Dapeng
Yu, Hailong
Wang, Qi
Han, Wenfeng
Guo, Mingming
author_facet Chen, Yu
Xiang, Liangbi
Liu, Jun
Zhou, Dapeng
Yu, Hailong
Wang, Qi
Han, Wenfeng
Guo, Mingming
author_sort Chen, Yu
collection PubMed
description Intrathecal injection of dynorphin into rats via subarachnoid catheter induces damage to spinal cord tissue and motor function. Injection of the kappa opioid receptor antagonist nor-binaltorphine, or the excitatory amino acid N-methyl-D-aspartate receptor antagonist MK-801 into rats alleviated the pathological changes of dynorphin-caused spinal cord tissue injury and reduced the acid phosphatase activity in the spinal cord. The experimental findings indicate that there are opioid and non-opioid pathways for dynorphin-induced spinal cord injury, and that the non-opioid receptor pathway may be mediated by the excitatory amino acid N-methyl-D-aspartate receptor.
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spelling pubmed-43427072015-03-03 A non-opioid pathway for dynorphin-caused spinal cord injury in rats☆ Chen, Yu Xiang, Liangbi Liu, Jun Zhou, Dapeng Yu, Hailong Wang, Qi Han, Wenfeng Guo, Mingming Neural Regen Res Research and Report: Spinal Cord Injury and Neuroregeneration Intrathecal injection of dynorphin into rats via subarachnoid catheter induces damage to spinal cord tissue and motor function. Injection of the kappa opioid receptor antagonist nor-binaltorphine, or the excitatory amino acid N-methyl-D-aspartate receptor antagonist MK-801 into rats alleviated the pathological changes of dynorphin-caused spinal cord tissue injury and reduced the acid phosphatase activity in the spinal cord. The experimental findings indicate that there are opioid and non-opioid pathways for dynorphin-induced spinal cord injury, and that the non-opioid receptor pathway may be mediated by the excitatory amino acid N-methyl-D-aspartate receptor. Medknow Publications & Media Pvt Ltd 2012-04-15 /pmc/articles/PMC4342707/ /pubmed/25737707 http://dx.doi.org/10.3969/j.issn.1673-5374.2012.11.003 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research and Report: Spinal Cord Injury and Neuroregeneration
Chen, Yu
Xiang, Liangbi
Liu, Jun
Zhou, Dapeng
Yu, Hailong
Wang, Qi
Han, Wenfeng
Guo, Mingming
A non-opioid pathway for dynorphin-caused spinal cord injury in rats☆
title A non-opioid pathway for dynorphin-caused spinal cord injury in rats☆
title_full A non-opioid pathway for dynorphin-caused spinal cord injury in rats☆
title_fullStr A non-opioid pathway for dynorphin-caused spinal cord injury in rats☆
title_full_unstemmed A non-opioid pathway for dynorphin-caused spinal cord injury in rats☆
title_short A non-opioid pathway for dynorphin-caused spinal cord injury in rats☆
title_sort non-opioid pathway for dynorphin-caused spinal cord injury in rats☆
topic Research and Report: Spinal Cord Injury and Neuroregeneration
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4342707/
https://www.ncbi.nlm.nih.gov/pubmed/25737707
http://dx.doi.org/10.3969/j.issn.1673-5374.2012.11.003
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