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Brain corticotropin‐releasing factor signaling: Involvement in acute stress‐induced visceral analgesia in male rats

Background Water avoidance stress (WAS) induces a naloxone‐independent visceral analgesia in male rats under non‐invasive conditions of monitoring. The objective of the study was to examine the role of brain CRF signaling in acute stress‐induced visceral analgesia (SIVA). Methods Adult male Sprague‐...

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Published in:Neurogastroenterology and motility 2019-02, Vol.31 (2), p.e13489-n/a
Main Authors: Larauche, Muriel, Moussaoui, Nabila, Biraud, Mandy, Bae, Won Ki, Duboc, Henri, Million, Mulugeta, Taché, Yvette
Format: Article
Language:English
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Summary:Background Water avoidance stress (WAS) induces a naloxone‐independent visceral analgesia in male rats under non‐invasive conditions of monitoring. The objective of the study was to examine the role of brain CRF signaling in acute stress‐induced visceral analgesia (SIVA). Methods Adult male Sprague‐Dawley rats were chronically implanted with an intracerebroventricular (ICV) cannula. The visceromotor response (VMR) to graded phasic colorectal distension (CRD: 10, 20, 40, 60 mm Hg, 20 seconds, 4 minutes intervals) was monitored using manometry. The VMR to a first CRD (baseline) was recorded 5 minutes after an ICV saline injection, followed 1 hour later by ICV injection of either CRF (30, 100, or 300 ng and 1, 3, or 5 μg/rat) or saline and a second CRD, 5 minutes later. Receptor antagonists against CRF1/CRF2 (astressin‐B, 30 μg/rat), CRF2 (astressin2‐B, 10 μg/rat), oxytocin (tocinoic acid, 20 μg/rat), or vehicle were injected ICV 5 minutes before CRF (300 ng/rat, ICV) or 15 minutes before WAS (1 hour). Key Results ICV CRF (100 and 300 ng) reduced the VMR to CRD at 60 mm Hg by −36.6% ± 6.8% and −48.7% ± 11.7%, respectively, vs baseline (P 
ISSN:1350-1925
1365-2982
DOI:10.1111/nmo.13489