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Upregulation of adrenomedullin in the spinal cord and dorsal root ganglia in the early phase of CFA-induced inflammation in rats.
Pain. 2009 Nov; 146(1-2):105-13.PAIN

Abstract

Adrenomedullin (AM), a member of calcitonin gene-related peptide (CGRP) family, has been demonstrated to be a pronociceptive mediator [28]. This study was undertaken to investigate the role of AM in a model of complete Freund's adjuvant (CFA)-induced inflammatory pain. Injection of CFA, but not of saline, in the unilateral hindpaw produced an increase in the expression of AM-like immunoreactivity (AM-IR) in laminae I-II of the spinal cord as well as in small- and medium-sized dorsal root ganglion (DRG) neurons at 48 h. The content of AM in DRG on the side ipsilateral to CFA injection started to increase at 4 h and remained at high levels at 24 and 48 h. The selective antagonist of AM receptors, AM(22-52), administered intrathecally (i.t.) 24 h after CFA injection inhibited inflammation-associated hyperalgesia in a dose-dependent manner (2, 5 and 10 nmol). Impressively, this anti-hyperalgesic effect lasted for at least 24 h. I.t. administration of AM(22-52) (10 nmol) also reversed CFA-induced increase in AM-IR in the spinal dorsal horn and DRG. Furthermore, blockade of AM receptors abolished CFA-induced changes in the expression and content of CGRP-like immunoreactivity in these regions. Taken together, our results suggest that the upregulation of AM in DRG neurons contributes to the development of inflammatory pain, and this effect is mediated, at least in part, by enhancing the expression and release of CGRP. Blocking AM receptor downstream signaling effects using antagonists has the potential of relieving pain following the induction of inflammation.

Authors+Show Affiliations

Provincial Key Laboratory of Developmental Biology and Neuroscience, Fujian Normal University, Fuzhou, Fujian 350108, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19683388

Citation

Hong, Yanguo, et al. "Upregulation of Adrenomedullin in the Spinal Cord and Dorsal Root Ganglia in the Early Phase of CFA-induced Inflammation in Rats." Pain, vol. 146, no. 1-2, 2009, pp. 105-13.
Hong Y, Liu Y, Chabot JG, et al. Upregulation of adrenomedullin in the spinal cord and dorsal root ganglia in the early phase of CFA-induced inflammation in rats. Pain. 2009;146(1-2):105-13.
Hong, Y., Liu, Y., Chabot, J. G., Fournier, A., & Quirion, R. (2009). Upregulation of adrenomedullin in the spinal cord and dorsal root ganglia in the early phase of CFA-induced inflammation in rats. Pain, 146(1-2), 105-13. https://doi.org/10.1016/j.pain.2009.07.015
Hong Y, et al. Upregulation of Adrenomedullin in the Spinal Cord and Dorsal Root Ganglia in the Early Phase of CFA-induced Inflammation in Rats. Pain. 2009;146(1-2):105-13. PubMed PMID: 19683388.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Upregulation of adrenomedullin in the spinal cord and dorsal root ganglia in the early phase of CFA-induced inflammation in rats. AU - Hong,Yanguo, AU - Liu,Yushan, AU - Chabot,Jean-Guy, AU - Fournier,Alain, AU - Quirion,Rémi, Y1 - 2009/08/14/ PY - 2008/12/23/received PY - 2009/07/06/revised PY - 2009/07/13/accepted PY - 2009/8/18/entrez PY - 2009/8/18/pubmed PY - 2009/12/31/medline SP - 105 EP - 13 JF - Pain JO - Pain VL - 146 IS - 1-2 N2 - Adrenomedullin (AM), a member of calcitonin gene-related peptide (CGRP) family, has been demonstrated to be a pronociceptive mediator [28]. This study was undertaken to investigate the role of AM in a model of complete Freund's adjuvant (CFA)-induced inflammatory pain. Injection of CFA, but not of saline, in the unilateral hindpaw produced an increase in the expression of AM-like immunoreactivity (AM-IR) in laminae I-II of the spinal cord as well as in small- and medium-sized dorsal root ganglion (DRG) neurons at 48 h. The content of AM in DRG on the side ipsilateral to CFA injection started to increase at 4 h and remained at high levels at 24 and 48 h. The selective antagonist of AM receptors, AM(22-52), administered intrathecally (i.t.) 24 h after CFA injection inhibited inflammation-associated hyperalgesia in a dose-dependent manner (2, 5 and 10 nmol). Impressively, this anti-hyperalgesic effect lasted for at least 24 h. I.t. administration of AM(22-52) (10 nmol) also reversed CFA-induced increase in AM-IR in the spinal dorsal horn and DRG. Furthermore, blockade of AM receptors abolished CFA-induced changes in the expression and content of CGRP-like immunoreactivity in these regions. Taken together, our results suggest that the upregulation of AM in DRG neurons contributes to the development of inflammatory pain, and this effect is mediated, at least in part, by enhancing the expression and release of CGRP. Blocking AM receptor downstream signaling effects using antagonists has the potential of relieving pain following the induction of inflammation. SN - 1872-6623 UR - https://www.unboundmedicine.com/medline/citation/19683388/Upregulation_of_adrenomedullin_in_the_spinal_cord_and_dorsal_root_ganglia_in_the_early_phase_of_CFA_induced_inflammation_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3959(09)00400-X DB - PRIME DP - Unbound Medicine ER -