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The effect of chemically induced colitis, psychological stress and their combination on visceral pain in female Wistar rats.
Stress 2014; 17(5):431-44S

Abstract

Visceral sensitivity is of pathophysiological importance in abdominal pain disorders and can be modulated by inflammation and stress. However, it is unclear whether inflammation and stress alter visceral perception independently of each other or in conjunction through neuroendocrine interactions. Therefore, we compared the short- and long-term effects of experimental colitis and water avoidance stress (WAS), alone or in combination, on visceral sensitivity in female Wistar rats. Colitis was induced by trinitrobenzene sulfonic acid (TNBS) and colonoscopically confirmed. During WAS, rats were placed on a platform surrounded by water for 1 h. Visceral sensitivity was assessed by quantifying the visceromotor responses (VMRs) to colorectal distension. Activation of the hypothalamic-pituitary-adrenal axis was determined by measuring serum corticosterone in a separate protocol. TNBS instillation resulted in overt colitis, associated with significant visceral hypersensitivity during the acute inflammatory phase (3 days post-TNBS; n = 8/group); after colitis had subsided (28 days post-TNBS), hypersensitivity was resolved (n = 4-8/group). Single WAS was associated with increased VMRs of a magnitude comparable to acute TNBS-induced hypersensitivity (n = 8/group). However, after repetitive WAS no significant hypersensitivity was present (n = 8/group). No additive effect of colitis and stress was seen on visceral pain perception (n = 6-8/group). Corticosterone levels were only increased in acute TNBS-colitis, acute WAS and their combination. To conclude, both colitis and stress successfully induced short-term visceral hypersensitivity and activated the hypothalamic-pituitary-adrenal axis, but long-term effects were absent. In addition, our current findings do not support an additive effect of colitis and stress on visceral sensitivity in female Wistar rats.

Authors+Show Affiliations

Laboratory of Experimental Medicine and Pediatrics, Division of Gastroenterology, University of Antwerp , Antwerp , Belgium and.No affiliation info availableNo 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

25089934

Citation

Deiteren, Annemie, et al. "The Effect of Chemically Induced Colitis, Psychological Stress and Their Combination On Visceral Pain in Female Wistar Rats." Stress (Amsterdam, Netherlands), vol. 17, no. 5, 2014, pp. 431-44.
Deiteren A, Vermeulen W, Moreels TG, et al. The effect of chemically induced colitis, psychological stress and their combination on visceral pain in female Wistar rats. Stress. 2014;17(5):431-44.
Deiteren, A., Vermeulen, W., Moreels, T. G., Pelckmans, P. A., De Man, J. G., & De Winter, B. Y. (2014). The effect of chemically induced colitis, psychological stress and their combination on visceral pain in female Wistar rats. Stress (Amsterdam, Netherlands), 17(5), pp. 431-44. doi:10.3109/10253890.2014.951034.
Deiteren A, et al. The Effect of Chemically Induced Colitis, Psychological Stress and Their Combination On Visceral Pain in Female Wistar Rats. Stress. 2014;17(5):431-44. PubMed PMID: 25089934.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The effect of chemically induced colitis, psychological stress and their combination on visceral pain in female Wistar rats. AU - Deiteren,Annemie, AU - Vermeulen,Wim, AU - Moreels,Tom G, AU - Pelckmans,Paul A, AU - De Man,Joris G, AU - De Winter,Benedicte Y, PY - 2014/8/5/entrez PY - 2014/8/5/pubmed PY - 2015/5/13/medline KW - Colorectal distension KW - inflammation KW - trinitrobenzene sulfonic acid KW - visceral hypersensitivity KW - visceromotor response KW - water avoidance stress SP - 431 EP - 44 JF - Stress (Amsterdam, Netherlands) JO - Stress VL - 17 IS - 5 N2 - Visceral sensitivity is of pathophysiological importance in abdominal pain disorders and can be modulated by inflammation and stress. However, it is unclear whether inflammation and stress alter visceral perception independently of each other or in conjunction through neuroendocrine interactions. Therefore, we compared the short- and long-term effects of experimental colitis and water avoidance stress (WAS), alone or in combination, on visceral sensitivity in female Wistar rats. Colitis was induced by trinitrobenzene sulfonic acid (TNBS) and colonoscopically confirmed. During WAS, rats were placed on a platform surrounded by water for 1 h. Visceral sensitivity was assessed by quantifying the visceromotor responses (VMRs) to colorectal distension. Activation of the hypothalamic-pituitary-adrenal axis was determined by measuring serum corticosterone in a separate protocol. TNBS instillation resulted in overt colitis, associated with significant visceral hypersensitivity during the acute inflammatory phase (3 days post-TNBS; n = 8/group); after colitis had subsided (28 days post-TNBS), hypersensitivity was resolved (n = 4-8/group). Single WAS was associated with increased VMRs of a magnitude comparable to acute TNBS-induced hypersensitivity (n = 8/group). However, after repetitive WAS no significant hypersensitivity was present (n = 8/group). No additive effect of colitis and stress was seen on visceral pain perception (n = 6-8/group). Corticosterone levels were only increased in acute TNBS-colitis, acute WAS and their combination. To conclude, both colitis and stress successfully induced short-term visceral hypersensitivity and activated the hypothalamic-pituitary-adrenal axis, but long-term effects were absent. In addition, our current findings do not support an additive effect of colitis and stress on visceral sensitivity in female Wistar rats. SN - 1607-8888 UR - https://www.unboundmedicine.com/medline/citation/25089934/The_effect_of_chemically_induced_colitis_psychological_stress_and_their_combination_on_visceral_pain_in_female_Wistar_rats_ L2 - http://www.tandfonline.com/doi/full/10.3109/10253890.2014.951034 DB - PRIME DP - Unbound Medicine ER -