Abdominal surgery-induced delayed gastric emptying in rats: role of CRF and sensory neurons

Barquist, Erik; Mj, Zinner; Rivier, Jean; Taché, Yvette

doi:10.1152/ajpgi.1992.262.4.g616

Cited by 45 publications

(56 citation statements)

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“…Pharmacological studies support the notion that gut CRF signaling occurs under stress (6,19,112,113). Several reports showed that the delayed gastric emptying induced by abdominal surgery can be blocked by peripheral injection of α-helical CRF 9-41 , d-Phe 12 CRF , and astressin (111,120,121). CRF 2 antagonists injected i.v.…”

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

confidence: 71%

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

Taché¹,

Bonaz²

2007

J. Clin. Invest.

317

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

confidence: 71%

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

Taché¹,

Bonaz²

2007

J. Clin. Invest.

317

285

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“…In the present study, the dose of ␣-helical CRF-(9-41) to induce a maximal effect is relatively low compared with previous studies (1,18,20), and we injected the antagonist into the cisterna magna, which is close to the medulla. Therefore, it can be suggested that the site of action for CRF antagonist is near the medulla, because CRF nerve terminals and receptors are located in the nuclei in this area (4).…”

Section: Table 4 Effect Of Intracisternal ␣-Helical Crf On Intracistmentioning

confidence: 78%

“…Previous reports showed that central CRF affects peripheral organs in part through the autonomic nervous system (29). In regard to the digestive system, central CRF inhibits gastric secretion and motility and exocrine secretion of the pancreas through the sympatheticnoradrenergic nervous system and the central CRF receptor antagonist partially reverses these effects (1,17,28). Meanwhile, we recently demonstrated that intracisternal injection of CRF aggravates CCl4-induced acute liver injury through the sympathetic-noradrenergic nervous system (33).…”

Section: Discussionmentioning

confidence: 91%

“…Some stressors or enhancement of the sympathetic nervous activity exacerbate experimental liver injury (6,(11)(12)(13)33). It has been shown that some physiological stressors increase CRF mRNA expression and CRF immunoreactivity in the hypothalamus and amygdala (8,15) and endogenous CRF regulates stress-induced alteration of the gastrointestinal functions through the autonomic nervous system (1,18,20). In this study, we investigated a role of endogenous CRF in hepatic pathophysiological regulations using CRF receptor antagonist ␣-helical CRF-(9-41) and demonstrated that ␣-helical CRF-(9-41) acts in the central nervous system and lessens CCl4-induced acute liver injury at least partially through the sympathetic-noradrenergic nervous system in rats.…”

Section: Table 4 Effect Of Intracisternal ␣-Helical Crf On Intracistmentioning

confidence: 99%

“…With respect to the gastrointestinal tract, central injection of CRF inhibited gastric motility and enhanced colonic motility through the autonomic nervous system (21,29). Physiological stressors are reported to increase CRF mRNA expression and CRF immunoreactivity in the hypothalamus and amygdala (8,15), and stress-induced alterations of gastrointestinal functions are abolished by central administration of a CRF receptor antagonist (1,18,20), suggesting involvement of endogenous CRF in these alterations of the gastrointestinal tract. In regard to the hepatobiliary system, the autonomic nervous system affects hepatic metabolism and hemodynamics (7,16).…”

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confidence: 99%

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Involvement of endogenous CRF in carbon tetrachloride-induced acute liver injury in rats

Nakade

Yoneda

Nakamura

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Central neuropeptides play important roles in many physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Central injection of corticotropin-releasing factor (CRF) aggravates carbon tetrachloride (CCl4)-induced acute liver injury through the sympathetic nervous pathway in rats. However, still nothing is known about a role of endogenous neuropeptides in the brain in hepatic pathophysiological regulations. Involvement of endogenous CRF in the brain in CCl4-induced acute liver injury was investigated by centrally injecting a CRF receptor antagonist in rats. Male fasted Wistar rats were injected with CRF receptor antagonist α-helical CRF-(9–41) (0.125–5 μg) intracisternally just before and 6 h after CCl4 (2 ml/kg) administration, and blood samples were obtained before and 24 h after CCl4 injection for measurement of hepatic enzymes. The liver sample was removed 24 h after CCl4 injection, and histological changes were examined. Intracisternal α-helical CRF-(9–41) dose dependently (0.25–2 μg) reduced the elevation of alanine aminotransferase and aspartate aminotransferase levels induced by CCl4. Intracisternal α-helical CRF-(9–41) reduced CCl4-induced liver histological changes, such as centrilobular necrosis. The effect of central CRF receptor antagonist on CCl4-induced liver injury was abolished by sympathectomy and 6-hydroxydopamine pretreatment but not by hepatic branch vagotomy or atropine pretreatment. These findings suggest the regulatory role of endogenous CRF in the brain in experimental liver injury in rats.

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Mechanisms and Treatment of Postoperative Ileus

Luckey¹

2003

Arch Surg

408

342

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To review the pathogenesis and treatment of postoperative ileus. Data Sources: Data collected for this review were identified from a MEDLINE database search of the Englishlanguage literature. The exact indexing terms were "postoperative ileus," "treatment," "etiology," and "pathophysiology." Previous review articles and pertinent references from those articles were also used. Study Selection: All relevant studies were included. Only articles that were case presentations or that mentioned postoperative ileus in passing were excluded.

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Abdominal surgery-induced delayed gastric emptying in rats: role of CRF and sensory neurons

Cited by 45 publications

References 0 publications

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

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

Involvement of endogenous CRF in carbon tetrachloride-induced acute liver injury in rats

Mechanisms and Treatment of Postoperative Ileus

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