{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T06:03:21Z","timestamp":1789193001329,"version":"build-2803163510"},"reference-count":55,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,2,26]],"date-time":"2012-02-26T00:00:00Z","timestamp":1330214400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2012,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background\u2002<\/jats:bold>Stress worsens abdominal pain experienced by patients with irritable bowel syndrome (IBS), a chronic disorder of unknown origin with comorbid anxiety. Previously, we have demonstrated colonic hypersensitivity in Wistar\u2013Kyoto rats (WKYs), a high\u2010anxiety strain, which models abdominal pain in IBS. In low\u2010anxiety rats, we have demonstrated that the central nucleus of the amygdala (CeA) regulates colonic hypersensitivity and anxiety induced by selective activation of either glucocorticoid receptors (GR) or mineralocorticoid receptors (MR), which is also mediated by the corticotropin releasing factor (CRF) Type\u20101 receptor. The goal of the present study was to test the hypothesis that the CeA through GR, MR, and\/or CRF\u20101R regulates colonic hypersensitivity in WKYs.<\/jats:p><jats:p><jats:bold>Methods\u2002<\/jats:bold>One series of WKYs had micropellets of a GR antagonist, an MR antagonist or cholesterol (control) stereotaxically implanted onto the CeA. Another series were infused in the CeA with CRF\u20101R antagonist, or vehicle. Colonic sensitivity was measured as a visceromotor response (VMR) to graded colorectal distension (CRD).<\/jats:p><jats:p><jats:bold>Key Results\u2002<\/jats:bold>The exaggerated VMR to graded CRD in WKYs was unaffected by GR or MR antagonism in the CeA. In contrast, direct CeA infusion of CRF\u20101R antagonist significantly inhibited the VMR to CRD at noxious distension pressures.<\/jats:p><jats:p><jats:bold>Conclusions &amp; Inferences\u2002<\/jats:bold>Stress hormones in the CeA regulate colonic hypersensitivity in the rat through strain\u2010dependent parallel pathways. The colonic hypersensitivity in WKYs is mediated by a CRF\u20101R mechanism in the CeA, independent of GR and MR. These complementary pathways suggest multiple etiologies whereby stress hormones in the CeA may regulate abdominal pain in IBS patients.<\/jats:p>","DOI":"10.1111\/j.1365-2982.2012.01899.x","type":"journal-article","created":{"date-parts":[[2012,2,27]],"date-time":"2012-02-27T01:49:54Z","timestamp":1330307394000},"page":"479-486","source":"Crossref","is-referenced-by-count":49,"title":["Importance of stress receptor\u2010mediated mechanisms in the amygdala on visceral pain perception in an intrinsically anxious rat"],"prefix":"10.1111","volume":"24","author":[{"given":"A. C.","family":"Johnson","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Tran","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Schulkin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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