학술논문

Red nucleus mGluR1 and mGluR5 facilitate the development of neuropathic pain through stimulating the expressions of TNF-α and IL-1β.
Document Type
Academic Journal
Author
Tian X; Department of Laboratory Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China; Department of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China; Shaanxi Blood Center, Xi'an, 710061, Shaanxi, China.; Wang WT; Department of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China.; Zhang MM; Department of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China.; Yang QQ; Department of Laboratory Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China; Department of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China.; Xu YL; Department of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China.; Wu JB; Department of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China.; Xie XX; Department of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China.; Wang JY; Department of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, Shaanxi, China. Electronic address: jywang@mail.xjtu.edu.cn.; Wang JY; Department of Laboratory Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China. Electronic address: wangjingyuan@xjtu.edu.cn.
Source
Publisher: Pergamon Press Country of Publication: England NLM ID: 8006959 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-9754 (Electronic) Linking ISSN: 01970186 NLM ISO Abbreviation: Neurochem Int Subsets: MEDLINE
Subject
Language
English
Abstract
Our previous study has identified that glutamate in the red nucleus (RN) facilitates the development of neuropathic pain through metabotropic glutamate receptors (mGluR). Here, we further explored the actions and possible molecular mechanisms of red nucleus mGluR Ⅰ (mGluR1 and mGluR5) in the development of neuropathic pain induced by spared nerve injury (SNI). Our data indicated that both mGluR1 and mGluR5 were constitutively expressed in the RN of normal rats. Two weeks after SNI, the expressions of mGluR1 and mGluR5 were significantly boosted in the RN contralateral to the nerve injury. Administration of mGluR1 antagonist LY367385 or mGluR5 antagonist MTEP to the RN contralateral to the nerve injury at 2 weeks post-SNI significantly ameliorated SNI-induced neuropathic pain. However, unilateral administration of mGluRⅠ agonist DHPG to the RN of normal rats provoked a significant mechanical allodynia, this effect could be blocked by LY367385 or MTEP. Further studies indicated that the expressions of TNF-α and IL-1β in the RN were also elevated at 2 weeks post-SNI. Administration of mGluR1 antagonist LY367385 or mGluR5 antagonist MTEP to the RN at 2 weeks post-SNI significantly inhibited the elevations of TNF-α and IL-1β. However, administration of mGluR Ⅰ agonist DHPG to the RN of normal rats significantly enhanced the expressions of TNF-α and IL-1β, these effects were blocked by LY367385 or MTEP. These results suggest that activation of red nucleus mGluR1 and mGluR5 facilitate the development of neuropathic pain by stimulating the expressions of TNF-α and IL-1β. mGluR Ⅰ maybe potential targets for drug development and clinical treatment of neuropathic pain.
Competing Interests: Declaration of competing interest The authors have approved the manuscript entitled “Red nucleus mGluR1 and mGluR5 facilitate the development of neuropathic pain through stimulating the expressions of TNF-α and IL-1β” and agreed with the submission to Neurochemistry International. All authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)