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Sosanya NM, Trevino AV, Chavez RL, et al. Sound-stress-induced altered nociceptive behaviors are associated with increased spinal CRFR2 gene expression in a rat model of burn injury. J Pain Res. 2017;10:2135-2145doi: 10.2147/JPR.S144055.
Sosanya, N. M., Trevino, A. V., Chavez, R. L., Christy, R. J., & Cheppudira, B. P. (2017). Sound-stress-induced altered nociceptive behaviors are associated with increased spinal CRFR2 gene expression in a rat model of burn injury. Journal of pain research, 102135-2145. https://doi.org/10.2147/JPR.S144055
Sosanya, Natasha M, et al. "Sound-stress-induced altered nociceptive behaviors are associated with increased spinal CRFR2 gene expression in a rat model of burn injury." Journal of pain research vol. 10 (2017): 2135-2145. doi: https://doi.org/10.2147/JPR.S144055
Sosanya NM, Trevino AV, Chavez RL, Christy RJ, Cheppudira BP. Sound-stress-induced altered nociceptive behaviors are associated with increased spinal CRFR2 gene expression in a rat model of burn injury. J Pain Res. 2017 Sep 01;10:2135-2145. doi: 10.2147/JPR.S144055. eCollection 2017. PMID: 28979159; PMCID: PMC5589110.
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J Pain Res. 2017 Sep 01;10:2135-2145. doi: 10.2147/JPR.S144055. eCollection 2017.

Sound-stress-induced altered nociceptive behaviors are associated with increased spinal CRFR2 gene expression in a rat model of burn injury.

Journal of pain research

Natasha M Sosanya, Alex V Trevino, Roger L Chavez, Robert J Christy, Bopaiah P Cheppudira

Affiliations

  1. United States Army Institute of Surgical Research, San Antonio Military Medical Center, Fort Sam Houston, San Antonio, TX, USA.

PMID: 28979159 PMCID: PMC5589110 DOI: 10.2147/JPR.S144055

Abstract

Sound stress (SS) elicits behavioral changes, including pain behaviors. However, the neuronal mechanisms underlying SS-induced pain behaviors remain to be explored. The current study examined the effects of SS on nociceptive behaviors and changes in expression of the spinal corticotropin-releasing factor (CRF) system in male Sprague Dawley rats with and without thermal pain. We also studied the effects of SS on plasma corticosterone and fecal output. Rats were exposed to 3 days of SS protocol (n = 12/group). Changes in nociceptive behaviors were assessed using thermal and mechanical pain tests. Following the induction of SS, a subgroup of rats (n = 6/group) was inflicted with thermal injury and on day 14 postburn nociceptive behaviors were reassessed. Spinal CRF receptor mRNA expression was analyzed by semiquantitative reverse transcription polymerase chain reaction (RT-PCR). In addition, plasma corticosterone and spinal CRF concentrations were quantified using enzyme-linked immunosorbent assay (ELISA). Increased defecation was observed in SS rats. SS produced transient mechanical allodynia in naive rats, whereas it exacerbated thermal pain in thermally injured rats. Spinal

Keywords: corticosterone; corticotropin-releasing factor receptor-2; mechanical pain; sound stress; thermal injury; thermal pain

Conflict of interest statement

Disclosure The opinions or assertions contained herein are the private views of the authors and are not to be considered as official or as reflecting the views of the Department of the Army or the Dep

References

  1. J Pain. 2009 Oct;10(10):1073-7 - PubMed
  2. Eur J Neurosci. 2015 Nov;42(10 ):2772-82 - PubMed
  3. Gen Comp Endocrinol. 2006 Mar;146(1):9-18 - PubMed
  4. Neuropharmacology. 2013 Sep;72:29-37 - PubMed
  5. Auton Neurosci. 2008 Aug 18;141(1-2):83-93 - PubMed
  6. J Neurochem. 2008 Oct;107(1):50-60 - PubMed
  7. Neurogastroenterol Motil. 2005 Jun;17(3):423-32 - PubMed
  8. Biomed Rep. 2015 Sep;3(5):703-706 - PubMed
  9. Neuropsychopharmacology. 2016 Sep;41(10 ):2463-72 - PubMed
  10. Prog Neurobiol. 2009 Jul;88(3):184-202 - PubMed
  11. Pain. 2006 Apr;121(3):241-60 - PubMed
  12. Mol Psychiatry. 1996 Sep;1(4):265-77 - PubMed
  13. J Neurosci. 2002 Apr 1;22(7):2926-35 - PubMed
  14. Psychoneuroendocrinology. 2009 May;34(4):587-96 - PubMed
  15. Noise Health. 2004 Jul-Sep;6(24):1-7 - PubMed
  16. Burns. 2015 Dec;41(8):1796-1804 - PubMed
  17. Eur J Pain. 2011 Sep;15(8):796-800 - PubMed
  18. Curr Mol Pharmacol. 2017 Feb 23;: - PubMed
  19. Virol J. 2011 Jan 09;8:7 - PubMed
  20. Am J Physiol Endocrinol Metab. 2005 Nov;289(5):E823-8 - PubMed
  21. Curr Top Behav Neurosci. 2014;20:251-80 - PubMed
  22. Am J Physiol Regul Integr Comp Physiol. 2006 Sep;291(3):R692-703 - PubMed
  23. Pain. 2013 Nov;154(11):2512-20 - PubMed
  24. Prog Neurobiol. 2014 Oct;121:1-18 - PubMed
  25. J Pain. 2008 Nov;9(11):991-8 - PubMed
  26. Eur Rev Med Pharmacol Sci. 2013 Nov;17(22):3060-7 - PubMed
  27. Arch Oral Biol. 2017 Jan;73:151-160 - PubMed
  28. J Neurosci Methods. 2006 Jul 15;155(1):122-5 - PubMed
  29. J Pain. 2015 Nov;16(11):1186-99 - PubMed
  30. Schriftenr Ver Wasser Boden Lufthyg. 2003;(112):5-79 - PubMed
  31. Neurotoxicology. 2017 Sep;62:151-161 - PubMed
  32. Gut. 2004 Jul;53(7):919-21 - PubMed
  33. Neurogastroenterol Motil. 2014 Nov;26(11):1605-14 - PubMed
  34. Front Neuroanat. 2017 Jun 26;11:49 - PubMed
  35. J Cell Biol. 2013 Jul 8;202(1):53-69 - PubMed
  36. Br J Pharmacol. 2004 Apr;141(8):1321-30 - PubMed
  37. Burns. 2014 Jun;40(4):759-71 - PubMed
  38. Pain. 2005 Jul;116(1-2):79-86 - PubMed
  39. Neuropsychopharmacology. 2007 Dec;32(12):2530-42 - PubMed

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