Corticotropin-Releasing Factor and the Brain-Gut Motor Response to Stress
The characterization of corticotropin-releasing factor (CRF) and CRF receptors, and the development of specific CRF receptor antagonists selective for the receptor subtypes have paved the way to the understanding of the biochemical coding of stress-related alterations of gut motor function. Reports...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1999-01-01
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| Series: | Canadian Journal of Gastroenterology |
| Online Access: | http://dx.doi.org/10.1155/1999/375916 |
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| Summary: | The characterization
of corticotropin-releasing factor (CRF) and CRF receptors,
and the development of specific CRF receptor antagonists
selective for the receptor subtypes have paved the way to the understanding
of the biochemical coding of stress-related alterations
of gut motor function. Reports have consistently established that
central administration of CRF acts in the brain to inhibit gastric
emptying while stimulating colonic motor function through modulation
of the vagal and sacral parasympathetic outflow in rodents.
Endogenous CRF in the brain plays a role in mediating various
forms of stressor-induced gastric stasis, including postoperative
gastric ileus, and activates colonic transit and fecal excretion elicited
by psychologically aversive or fearful stimuli. It is known that
brain CRF is involved in the cross-talk between the immune and
gastrointestinal systems because systemic or central administration
of interleukin-1-beta delays gastric emptying while stimulating
colonic motor activity through activation of CRF release in
the brain. The paraventricular nucleus of the hypothalamus and
the dorsal vagal complex are important sites of action for CRF to
inhibit gastric motor function, while the paraventricular nucleus
of the hypothalamus and the locus coeruleus complex are sites of
action for CRF to stimulate colonic motor function. The inhibition
of gastric emptying by CRF may be mediated by the interaction
with the CRF2 receptors, while the anxiogenic and colonic
motor responses may involve CRF1 receptors. Hypersecretion of
CRF in the brain may contribute to the pathophysiology of
stress-related exacerbation of irritable bowel syndrome. |
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| ISSN: | 0835-7900 |