Spinal changes of a newly isolated neuropeptide endomorphin-2 concomitant with vincristine-induced allodynia

Chemotherapy-induced neuropathic pain (CNP) is the major dose-limiting factor in cancer chemotherapy. However, the neural mechanisms underlying CNP remain unclear. There is increasing evidence implicating the involvement of spinal endomorphin-2 (EM2) in neuropathic pain. In this study, we used a vin...

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Published in:PloS one 2014-02, Vol.9 (2), p.e89583
Main Authors: Yang, Yang, Zhang, Yong-Gang, Lin, Guo-An, Xie, He-Qiu, Pan, Hai-Tao, Huang, Ben-Qing, Liu, Ji-Dong, Liu, Hui, Zhang, Nan, Li, Li, Chen, Jian-Hua
Format: Article
Language:English
Subjects:
Analgesia
Analgesics
Analysis
Animals
Antineoplastic Agents, Phytogenic - toxicity
Biology
Cancer
Chemotherapy
Dipeptidyl-peptidase IV
Dipeptidyl-Peptidases and Tripeptidyl-Peptidases - metabolism
Drug dosages
Electrophysiology
Endogenous opioids
Endomorphin-2
Fluorescent Antibody Technique
Hyperalgesia - chemically induced
Hyperalgesia - metabolism
Hyperalgesia - pathology
Immunoblotting
Immunoenzyme Techniques
Injections, Spinal
Ligands
Male
Medicine
Metabolism
Narcotics
Neuralgia
Neuralgia - chemically induced
Neuralgia - metabolism
Neuralgia - pathology
Neuropathy
Neurosciences
Neurosurgery
Oligopeptides - metabolism
Opioid receptors (type mu)
Oxidative stress
Pain
Pain perception
Peptides
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species - metabolism
Rodents
Spinal cord
Spinal Cord - drug effects
Spinal Cord - metabolism
Studies
Vincristine
Vincristine - toxicity
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cited_by cdi_FETCH-LOGICAL-c692t-aebb18903b295648ca55f7b95b6dac8bb9e9490421c9ede296a9dbb143b05e093
cites cdi_FETCH-LOGICAL-c692t-aebb18903b295648ca55f7b95b6dac8bb9e9490421c9ede296a9dbb143b05e093
container_end_page
container_issue 2
container_start_page e89583
container_title PloS one
container_volume 9
creator Yang, Yang
Zhang, Yong-Gang
Lin, Guo-An
Xie, He-Qiu
Pan, Hai-Tao
Huang, Ben-Qing
Liu, Ji-Dong
Liu, Hui
Zhang, Nan
Li, Li
Chen, Jian-Hua
description Chemotherapy-induced neuropathic pain (CNP) is the major dose-limiting factor in cancer chemotherapy. However, the neural mechanisms underlying CNP remain unclear. There is increasing evidence implicating the involvement of spinal endomorphin-2 (EM2) in neuropathic pain. In this study, we used a vincristine-evoked rat CNP model displaying mechanical allodynia and central sensitization, and observed a significant decrease in the expression of spinal EM2 in CNP. Also, while intrathecal administration of exogenous EM2 attenuated allodynia and central sensitization, the mu-opioid receptor antagonist β-funaltrexamine facilitated these events. We found that the reduction in spinal EM2 was mediated by increased activity of dipeptidylpeptidase IV, possibly as a consequence of chemotherapy-induced oxidative stress. Taken together, our findings suggest that a decrease in spinal EM2 expression causes the loss of endogenous analgesia and leads to enhanced pain sensation in CNP.
doi_str_mv 10.1371/journal.pone.0089583
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However, the neural mechanisms underlying CNP remain unclear. There is increasing evidence implicating the involvement of spinal endomorphin-2 (EM2) in neuropathic pain. In this study, we used a vincristine-evoked rat CNP model displaying mechanical allodynia and central sensitization, and observed a significant decrease in the expression of spinal EM2 in CNP. Also, while intrathecal administration of exogenous EM2 attenuated allodynia and central sensitization, the mu-opioid receptor antagonist β-funaltrexamine facilitated these events. We found that the reduction in spinal EM2 was mediated by increased activity of dipeptidylpeptidase IV, possibly as a consequence of chemotherapy-induced oxidative stress. Taken together, our findings suggest that a decrease in spinal EM2 expression causes the loss of endogenous analgesia and leads to enhanced pain sensation in CNP.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24586889</pmid><doi>10.1371/journal.pone.0089583</doi><tpages>e89583</tpages><oa>free_for_read</oa></addata></record>
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source Publicly Available Content Database; PubMed Central
subjects Analgesia
Analgesics
Analysis
Animals
Antineoplastic Agents, Phytogenic - toxicity
Biology
Cancer
Chemotherapy
Dipeptidyl-peptidase IV
Dipeptidyl-Peptidases and Tripeptidyl-Peptidases - metabolism
Drug dosages
Electrophysiology
Endogenous opioids
Endomorphin-2
Fluorescent Antibody Technique
Hyperalgesia - chemically induced
Hyperalgesia - metabolism
Hyperalgesia - pathology
Immunoblotting
Immunoenzyme Techniques
Injections, Spinal
Ligands
Male
Medicine
Metabolism
Narcotics
Neuralgia
Neuralgia - chemically induced
Neuralgia - metabolism
Neuralgia - pathology
Neuropathy
Neurosciences
Neurosurgery
Oligopeptides - metabolism
Opioid receptors (type mu)
Oxidative stress
Pain
Pain perception
Peptides
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species - metabolism
Rodents
Spinal cord
Spinal Cord - drug effects
Spinal Cord - metabolism
Studies
Vincristine
Vincristine - toxicity
title Spinal changes of a newly isolated neuropeptide endomorphin-2 concomitant with vincristine-induced allodynia
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T17%3A56%3A57IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Spinal%20changes%20of%20a%20newly%20isolated%20neuropeptide%20endomorphin-2%20concomitant%20with%20vincristine-induced%20allodynia&rft.jtitle=PloS%20one&rft.au=Yang,%20Yang&rft.date=2014-02-24&rft.volume=9&rft.issue=2&rft.spage=e89583&rft.pages=e89583-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0089583&rft_dat=%3Cgale_plos_%3EA478794110%3C/gale_plos_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c692t-aebb18903b295648ca55f7b95b6dac8bb9e9490421c9ede296a9dbb143b05e093%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1501614189&rft_id=info:pmid/24586889&rft_galeid=A478794110&rfr_iscdi=true