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 language | English (US) |
|---|---|
| Pages (from-to) | 29-37 |
| Number of pages | 9 |
| Journal | Neuropharmacology |
| Volume | 72 |
| DOIs | |
| State | Published - 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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