Tags

Type your tag names separated by a space and hit enter

Importance of stress receptor-mediated mechanisms in the amygdala on visceral pain perception in an intrinsically anxious rat.
Neurogastroenterol Motil 2012; 24(5):479-86, e219NM

Abstract

BACKGROUND

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-Kyoto rats (WKYs), a high-anxiety strain, which models abdominal pain in IBS. In low-anxiety 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-1 receptor. The goal of the present study was to test the hypothesis that the CeA through GR, MR, and/or CRF-1R regulates colonic hypersensitivity in WKYs.

METHODS

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-1R antagonist, or vehicle. Colonic sensitivity was measured as a visceromotor response (VMR) to graded colorectal distension (CRD).

KEY RESULTS

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-1R antagonist significantly inhibited the VMR to CRD at noxious distension pressures.

CONCLUSIONS & INFERENCES

Stress hormones in the CeA regulate colonic hypersensitivity in the rat through strain-dependent parallel pathways. The colonic hypersensitivity in WKYs is mediated by a CRF-1R 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.

Authors+Show Affiliations

Oklahoma Center for Neuroscience, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

22364507

Citation

Johnson, A C., et al. "Importance of Stress Receptor-mediated Mechanisms in the Amygdala On Visceral Pain Perception in an Intrinsically Anxious Rat." Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society, vol. 24, no. 5, 2012, pp. 479-86, e219.
Johnson AC, Tran L, Schulkin J, et al. Importance of stress receptor-mediated mechanisms in the amygdala on visceral pain perception in an intrinsically anxious rat. Neurogastroenterol Motil. 2012;24(5):479-86, e219.
Johnson, A. C., Tran, L., Schulkin, J., & Greenwood-Van Meerveld, B. (2012). Importance of stress receptor-mediated mechanisms in the amygdala on visceral pain perception in an intrinsically anxious rat. Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society, 24(5), pp. 479-86, e219. doi:10.1111/j.1365-2982.2012.01899.x.
Johnson AC, et al. Importance of Stress Receptor-mediated Mechanisms in the Amygdala On Visceral Pain Perception in an Intrinsically Anxious Rat. Neurogastroenterol Motil. 2012;24(5):479-86, e219. PubMed PMID: 22364507.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Importance of stress receptor-mediated mechanisms in the amygdala on visceral pain perception in an intrinsically anxious rat. AU - Johnson,A C, AU - Tran,L, AU - Schulkin,J, AU - Greenwood-Van Meerveld,B, Y1 - 2012/02/26/ PY - 2012/2/28/entrez PY - 2012/3/1/pubmed PY - 2012/8/3/medline SP - 479-86, e219 JF - Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society JO - Neurogastroenterol. Motil. VL - 24 IS - 5 N2 - BACKGROUND: 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-Kyoto rats (WKYs), a high-anxiety strain, which models abdominal pain in IBS. In low-anxiety 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-1 receptor. The goal of the present study was to test the hypothesis that the CeA through GR, MR, and/or CRF-1R regulates colonic hypersensitivity in WKYs. METHODS: 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-1R antagonist, or vehicle. Colonic sensitivity was measured as a visceromotor response (VMR) to graded colorectal distension (CRD). KEY RESULTS: 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-1R antagonist significantly inhibited the VMR to CRD at noxious distension pressures. CONCLUSIONS & INFERENCES: Stress hormones in the CeA regulate colonic hypersensitivity in the rat through strain-dependent parallel pathways. The colonic hypersensitivity in WKYs is mediated by a CRF-1R 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. SN - 1365-2982 UR - https://www.unboundmedicine.com/medline/citation/22364507/Importance_of_stress_receptor_mediated_mechanisms_in_the_amygdala_on_visceral_pain_perception_in_an_intrinsically_anxious_rat_ L2 - https://doi.org/10.1111/j.1365-2982.2012.01899.x DB - PRIME DP - Unbound Medicine ER -