Central regulation of gastric emptying of solid nutrient meals by corticotropin releasing factor

Lee, C.; Sarna, S. K.

doi:10.1046/j.1365-2982.1997.d01-58.x

Cited by 36 publications

(29 citation statements)

References 20 publications

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“…In those experiments, injection of CRF or Ucn 1 induced an increase in the contractile activity of the duodenum but inhibited the percentage of propagated duodenal contractions (21,23). These effects of CRF or Ucn 1 on the duodenal contractile activity are in agreement with the present results, in which CRF or Ucn 1 elicited an increase of the duodenal smooth muscle contractions.…”

Section: Discussionsupporting

confidence: 82%

“…Functional experiments showed that, in vivo, central or peripheral administration of CRF or Ucn 1 inhibited gastric emptying, delayed small intestinal transit, and stimulated colonic transit (21,23,31,57,58). In those experiments, injection of CRF or Ucn 1 induced an increase in the contractile activity of the duodenum but inhibited the percentage of propagated duodenal contractions (21,23).…”

Section: Discussionmentioning

confidence: 99%

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Expression and effects of metabotropic CRF₁and CRF₂receptors in rat small intestine

Porcher¹,

Juhem²,

Peinnequin³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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Porcher, Christophe, Aurélie Juhem, André Peinnequin, Valé-rie Sinniger, and Bruno Bonaz. Expression and effects of metabotropic CRF1 and CRF2 receptors in rat small intestine. Am J Physiol Gastrointest Liver Physiol 288: G1091-G1103, 2005. First published January 6, 2005; doi:10.1152/ajpgi.00302.2004.-Corticotropin-releasing factor (CRF)-like peptides mediate their effects via two receptor subtypes, CRF1 and CRF2; these receptors have functional implication in the motility of the stomach and colon in rats. We evaluated expression and functions of CRF1 and CRF2 receptors in the rat small intestine (i.e., duodenum and ileum). CRF1-2-like immunoreactivity (CRF1-2-LI) was localized in fibers and neurons of the myenteric and submucosal ganglia. CRF1-2-LI was found in nerve fibers of the longitudinal and circular muscle layers, in the mucosa, and in mucosal cells. Quantitative RT-PCR showed a stronger expression of CRF2 than CRF1 in the ileum, whereas CRF1 expression was higher than CRF2 expression in the duodenum. Functional studies showed that CRF-like peptides increased duodenal phasic contractions and reduced ileal contractions. CRF1 antagonists (CP-154,526 and SSR125543Q) blocked CRF-like peptide-induced activation of duodenal motility but did not block CRF-like peptide-induced inhibition of ileal motility. In contrast, a CRF2 inhibitor (astressin2-B) blocked the effects of CRF-like peptides on ileal muscle contractions but did not influence CRF-like peptide-induced activation of duodenal motility. These results demonstrate the presence of CRF1-2 in the intestine and demonstrate that, in vitro, CRF-like peptides stimulate the contractile activity of the duodenum through CRF1 receptor while inhibiting phasic contractions of the ileum through CRF2 receptor. These results strongly suggest that CRF-like peptides play a major role in the regulatory mechanisms that underlie the neural control of small intestinal motility through CRF receptors. astressin2-B; corticotropin-releasing factor receptors; urocortin CORTICOTROPIN-RELEASING FACTOR (CRF) is a 41-amino acid peptide recognized as a major regulator of pituitary adrenocorticotropin (54). This neuropeptide is the principal mediator of a wide variety of physiological responses caused by sustained stresses (2, 9, 22, 51). The paraventricular nucleus (PVN) of the hypothalamus is the main source for CRF in the brain (49). Recently, the addition of three mammalian neuropeptides, urocortin (Ucn) 1, Ucn 2, and Ucn 3, have expanded the family of CRF-related peptides (18).The CRF-like peptides mediate their effects via two receptor subtypes, CRF 1 and CRF 2␣ /CRF 2␤ , each encoded by distinct genes (6,8,27,41). Both receptors belong to the seventransmembrane domain family positively coupled to adenylate cyclase via G proteins (1,3,12). CRF 1 receptor mRNA is predominantly expressed in the brain under basal conditions (4, 45) but is increased in the PVN in acute stress (4), somatovisceral pain (50), and colitis (42). The distribution of the CRF 2 receptor variants differs by ...

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Expression and effects of metabotropic CRF₁and CRF₂receptors in rat small intestine

Porcher¹,

Juhem²,

Peinnequin³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Removal of the pituitary gland or adrenal glands had no effect on CRF inhibition of gastric emptying; this indicates that the gastric effect is not secondary to the activation of the HPA axis (61,62). All reports, except 2 (61, 63), have identified the vagus nerve as the main pathway mediating the delayed gastric transit and inhibition of gastric motility induced by central injection of either CRF or urocortin 1 in rats and dogs (54,55,57,59,62,64,65). By contrast, the delayed gastric emptying induced by injection of urocortin 2 into the CSF is not altered by gastric vagotomy and instead requires the integrity of the sympathetic nervous system and peripheral α-adrenergic receptors (57).…”

Section: Link Between Crf Receptors In the Brain And Stressrelated Almentioning

confidence: 99%

“…CRF, urocortin 1, urocortin 2, and the nonmammalian CRF-related peptides sauvagine and urotensin I inhibit gastric emptying of noncaloric liquid, caloric liquid, and solid food when injected into the cerebrospinal fluid (CSF) of several nonprimate mammals (53). These peptides also inhibit basal and cholinergic-stimulated gastric motility in rodents and dogs (54,55). CRF 2 is the CRF receptor subtype in the brain through which CRF and urocortins injected into the CSF primarily initiate their inhibitory effect on gastric transit and motility (56)(57)(58).…”

Section: Link Between Crf Receptors In the Brain And Stressrelated Almentioning

confidence: 99%

Corticotropin-releasing factor receptors and stress-related alterations of gut motor function

Taché¹,

Bonaz²

2007

J. Clin. Invest.

314

285

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Over the past few decades, corticotropin-releasing factor (CRF) signaling pathways have been shown to be the main coordinators of the endocrine, behavioral, and immune responses to stress. Emerging evidence also links the activation of CRF receptors type 1 and type 2 with stress-related alterations of gut motor function. Here, we review the role of CRF receptors in both the brain and the gut as part of key mechanisms through which various stressors impact propulsive activity of the gastrointestinal system. We also examine how these mechanisms translate into the development of new approaches for irritable bowel syndrome, a multifactorial disorder for which stress has been implicated in the pathophysiology. Stress and gut motor functionA real or perceived threat to the homeostasis of mammalian organisms, originating internally or externally, triggers adaptive stress responses that affect behavior, as well as endocrine, immune, autonomic, and visceral functions (1, 2). Regarding effects in visceral functions in particular, early seminal investigations reported by Cannon and by Almy and colleagues provided clear evidence that emotional stress impacts gastric and colonic motor activity in healthy volunteers and cats (3, 4). Subsequent studies established that delayed emptying of the stomach is the most common response evoked by various acute stressors in both experimental animals and healthy human subjects (5). By contrast, in the colon, various stressors (including anxiety, dichotomous listening, fear, intermittent hand immersion in cold water, and stressful interviews) increase colonic motility in healthy subjects (5). Similarly, in rodents and dogs, stressors as diverse as open-field test, fear conditioning, loud sound, restraint, cold exposure, water avoidance, inescapable foot or tail shocks, and increased levels of cytokines induced by endotoxins stimulate propulsive colonic motor function (2, 5-7). The autonomic nervous system provides a peripheral neuronal network by which the effects of stress can be rapidly imposed on gut function. These are mediated through the sympathetic, and vagal and pelvic parasympathetic innervation of the enteric nervous system embedded into the muscular layers of the gut (8).It is becoming increasingly recognized that these interconnected brain-gut neuronal pathways activated during stress have relevance in the pathophysiology of functional bowel disorders (9-11). In particular, various stressors in the form of early life trauma, sexual abuse, maternal neglect, fear conditioning, lifethreatening events, and enteric infection have an important role in the etiology of irritable bowel syndrome (IBS), which is characterized by altered bowel movements, bloating, and visceral pain (10-13). Cyclic vomiting syndrome is another brain-gut disorder manifested by recurrent, stereotyped episodes of nausea and vomiting in the pediatric population, which is triggered by stressors related to heightened emotional state, fasting, exercise, and infection in 80% of the patients (14).A big step forward...

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“…One physiological effect of stress is the inhibition of digestive function, a mechanism that allows animals to divert blood flow and energy reserves to organs essential for dealing with the stressor. Stress-induced alterations to digestive physiology that have garnered the most empirical attention include inhibition of gastrointestinal motility (Coskun et al 1997;Lee & Sarna 1997;Plourde 1999;Taché et al 1999) and the acceleration of colonic transit (Mönnikes et al 1993). These effects are mediated by corticotropin-releasing factor (CRF), a neuropeptide at the apex of the neuroendocrine stress axis (Mö nnikes et al 1993;Taché et al 1999).…”

Section: Introductionmentioning

confidence: 99%

The gall of subordination: changes in gall bladder function associated with social stress

Earley

Blumer

Grober

2004

Proc. R. Soc. Lond. B

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Diverse physiological and behavioural mechanisms allow animals to effectively deal with stressors, but chronic activation of the stress axis can have severe consequences. We explored the effects of chronic social stress on agonistic behaviour and gall bladder function, a critical but widely neglected component of stress-induced gastrointestinal dysfunction. Prolonged cohabitation with dominant individuals elicited behavioural modifications and dramatically increased bile retention in subordinate convict cichlid fish (Archocentrus nigrofasciatum). The key predictor of gall bladder hypertrophy was social subordination rather than status-related differences in food intake or body size. Stress-induced inhibition of gall bladder emptying could affect energy assimilation such that subordinate animals would not be able to effectively convert energy-rich food into mass gain. These results parallel changes in gall bladder function preceding cholesterol gallstone formation in humans and other mammals. Thus, social stress may be an important diagnostic criterion in understanding pathologies associated with gall bladder dysfunction.

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Central regulation of gastric emptying of solid nutrient meals by corticotropin releasing factor

Cited by 36 publications

References 20 publications

Expression and effects of metabotropic CRF₁and CRF₂receptors in rat small intestine

Expression and effects of metabotropic CRF₁and CRF₂receptors in rat small intestine

Corticotropin-releasing factor receptors and stress-related alterations of gut motor function

The gall of subordination: changes in gall bladder function associated with social stress

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Central regulation of gastric emptying of solid nutrient meals by corticotropin releasing factor

Cited by 36 publications

References 20 publications

Expression and effects of metabotropic CRF1and CRF2receptors in rat small intestine

Expression and effects of metabotropic CRF1and CRF2receptors in rat small intestine

Corticotropin-releasing factor receptors and stress-related alterations of gut motor function

The gall of subordination: changes in gall bladder function associated with social stress

Contact Info

Product

Resources

About

Expression and effects of metabotropic CRF₁and CRF₂receptors in rat small intestine

Expression and effects of metabotropic CRF₁and CRF₂receptors in rat small intestine