Forced swim-induced musculoskeletal hyperalgesia is mediated by CRF2 receptors but not by TRPV1 receptors

Ramy E. Abdelhamid, Katalin J. Kovacs, Jeffrey D. Pasley, Myra G. Nunez, Alice A. Larson

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

The exacerbation of musculoskeletal pain by stress in humans is modeled by the musculoskeletal hyperalgesia in rodents following a forced swim. We hypothesized that stress-sensitive corticotropin releasing factor (CRF) receptors and transient receptor vanilloid 1 (TRPV1) receptors are responsible for the swim stress-induced musculoskeletal hyperalgesia. We confirmed that a cold swim (26 °C) caused a transient, morphine-sensitive decrease in grip force responses reflecting musculoskeletal hyperalgesia in mice. Pretreatment with the CRF2 receptor antagonist astressin 2B, but not the CRF1 receptor antagonist NBI-35965, attenuated this hyperalgesia. Desensitizing the TRPV1 receptor centrally or peripherally using desensitizing doses of resiniferatoxin (RTX) failed to prevent the musculoskeletal hyperalgesia produced by cold swim. SB-366791, a TRPV1 antagonist, also failed to influence swim-induced hyperalgesia. Together these data indicate that swim stress-induced musculoskeletal hyperalgesia is mediated, in part, by CRF2 receptors but is independent of the TRPV1 receptor.

Original languageEnglish (US)
Pages (from-to)29-37
Number of pages9
JournalNeuropharmacology
Volume72
DOIs
StatePublished - 2013

Bibliographical note

Funding Information:
This work was supported by a grant from NIH from the National Institutes on Arthritis and Musculoskeletal and Skin Diseases [ AR056092 ].

Keywords

  • CRF
  • Forced swim
  • Hyperalgesia
  • RTX
  • Stress
  • TRPV1
  • Urocortin

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