Peripheral and central administration of exogenous urocortin 1 disrupts the fasted motility pattern of the small intestine in rats via the corticotrophin releasing factor receptor 2 and a cholinergic mechanism

Yin, Yan; Dong, Lei; Yin, Dong Min

doi:10.1111/j.1440-1746.2007.05142.x

Cited by 5 publications

(4 citation statements)

References 48 publications

(104 reference statements)

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“…Although blockage of peripheral CRFr2 was carried on in our study, results from other researchers indicate that peripheral CRFr2 also plays an important role in mediating the stress response following central and peripheral injections of CRF and its related peptides, leading to abnormal motility in the small intestine. 24 Therefore, the improved jejunal dysmotility following EA treatment can also probably be ascribed to the regulation of peripheral CRFr2 in the jejunum.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture ameliorates corticotrophin-releasing factor-induced jejunal dysmotility in a rat model of stress

et al. 2020

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Background Central injection of corticotrophin-releasing factor (CRF) mimics the effect of stress on gastrointestinal (GI) responses, including inhibition of GI motility. This study was designed to explore the effects of electroacupuncture (EA) on disordered jejunal motility in a rat model of stress induced by intracisternal (IC) injection of CRF. Methods A stress model was established by IC injection of CRF in Sprague–Dawley rats. GI motility was evaluated by assessing gastric emptying (GE), gastrointestinal transit (GIT) and jejunal motility in vivo. EA was performed at ST36. The functional roles of CRF receptor subtype 1 and subtype 2 (CRFr1 and CRFr2) were examined by IC administration of the corresponding selective CRF antagonists. Protein expression of CRFr1 and CRFr2 in the hypothalamus and jejunum was detected by Western blotting. Results IC injection of CRF significantly inhibited GE, GIT and jejunal motility. EA treatment remarkably improved the disturbed GI motility. Intriguingly, the disordered jejunal motility induced by central CRF was abolished by IC injection of a selective CRFr2 antagonist, indicating the essential role of central CRFr2 in mediating the stress-induced jejunal motor disorder. EA at ST36 decreased central and peripheral expression of CRFr2, which might be one of the potential mechanisms underlying the beneficial effect of EA on jejunal dysmotility in this rat model of stress. Conclusion This study suggested that EA at ST36 could ameliorate disordered jejunal motility induced by stress, and that this might be associated with the down-regulation of CRFr2.

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Section: Discussionmentioning

confidence: 99%

Electroacupuncture ameliorates corticotrophin-releasing factor-induced jejunal dysmotility in a rat model of stress

et al. 2020

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“…These data provide convergent pharmacological evidence for a role of peripheral Ucns/CRF 2 signaling pathways in the alterations of gastric propulsive motor function induced by acute exposure to physical/visceral stressors. However, contrary to the wealth of functional studies on the actions of Ucns and potential relevance of Ucns/CRF 2 signaling in the stomach in experimental animals and humans (3,10,33,69), little is known about the expression and regulation of Ucn ligands and CRF 2 receptors within the various gastric corpus (GC) layers compared with reports in other gut segments (7,8) or visceral organs such as the heart (31).…”

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confidence: 98%

Urocortins and CRF type 2 receptor isoforms expression in the rat stomach are regulated by endotoxin: role in the modulation of delayed gastric emptying

Yuan

Taché

2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Peripheral activation of corticotropin-releasing factor receptor type 2 (CRF2) by urocortin 1, 2, or 3 (Ucns) exerts powerful effects on gastric function; however, little is known about their expression and regulation in the stomach. We investigated the expression of Ucns and CRF2 isoforms by RT-PCR in the gastric corpus (GC) mucosa and submucosa plus muscle (S+M) or laser captured layers in naive rats, their regulations by lipopolysaccharide (LPS, 100 μg/kg ip) over 24 h, and the effect of the CRF2 antagonist astresssin2-B (100 μg/kg sc) on LPS-induced delayed gastric emptying (GE) 2-h postinjection. Transcripts of Ucns and CRF2b, the most common wild-type CRF2 isoform in the periphery, were expressed in all layers, including myenteric neurons. LPS increased Ucn mRNA levels significantly in both mucosa and S+M, reaching a maximal response at 6 h postinjection and returning to basal levels at 24 h except for Ucn 1 in S+M. By contrast, CRF2b mRNA level was significantly decreased in the mucosa and M+S with a nadir at 6 h. In addition, CRF2a, reportedly only found in the brain, and the novel splice variant CRF2a-3 were also detected in the GC, antrum, and pylorus. LPS reciprocally regulated these variants with a decrease of CRF2a and an increase of CRF2a-3 in the GC 6 h postinjection. Astressin2-B exacerbated LPS-delayed GE (42–73%, P < 0.001). These data indicate that Ucn and CRF2 isoforms are widely distributed throughout the rat stomach and inversely regulated by immune stress. The CRF2 signaling system may act to counteract the early gastric motor alterations to endotoxemia.

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“…Nonetheless, a combination of repeated environmental stressors may lead to a maladaptive response resulting in altered brain structure and function (35), predisposing to disease. CRH receptors are found to be expressed in both the GI tract and the central nervous system (CNS) suggesting a crucial role for this factor in the stress-induced disruption of gut homeostasis (36) including transit (37)(38)(39), visceral sensitivity (40)(41)(42), intestinal permeability (36,43,44) and gastric inflammation (45). Psychological stress and anxiety, often reported by FGID patients, influence the onset of symptoms and predict the clinical outcome (46).…”

Section: Stress-related Models Of Fgidmentioning

confidence: 99%

Animal Models for Functional Gastrointestinal Disorders

Accarie

Vanuytsel

2020

Front. Psychiatry

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Functional gastrointestinal disorders (FGID), such as functional dyspepsia (FD) and irritable bowel syndrome (IBS) are characterized by chronic abdominal symptoms in the absence of an organic, metabolic or systemic cause that readily explains these complaints. Their pathophysiology is still not fully elucidated and animal models have been of great value to improve the understanding of the complex biological mechanisms. Over the last decades, many animal models have been developed to further unravel FGID pathophysiology and test drug efficacy. In the first part of this review, we focus on stress-related models, starting with the different perinatal stress models, including the stress of the dam, followed by a discussion on neonatal stress such as the maternal separation model. We also describe the most commonly used stress models in adult animals which brought valuable insights on the brain-gut axis in stress-related disorders. In the second part, we focus more on models studying peripheral, i.e., gastrointestinal, mechanisms, either induced by an infection or another inflammatory trigger. In this section, we also introduce more recent models developed around food-related metabolic disorders or food hypersensitivity and allergy. Finally, we introduce models mimicking FGID as a secondary effect of medical interventions and spontaneous models sharing characteristics of GI and anxiety-related disorders. The latter are powerful models for brain-gut axis dysfunction and bring new insights about FGID and their comorbidities such as anxiety and depression.

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Peripheral and central administration of exogenous urocortin 1 disrupts the fasted motility pattern of the small intestine in rats via the corticotrophin releasing factor receptor 2 and a cholinergic mechanism

Cited by 5 publications

References 48 publications

Electroacupuncture ameliorates corticotrophin-releasing factor-induced jejunal dysmotility in a rat model of stress

Electroacupuncture ameliorates corticotrophin-releasing factor-induced jejunal dysmotility in a rat model of stress

Urocortins and CRF type 2 receptor isoforms expression in the rat stomach are regulated by endotoxin: role in the modulation of delayed gastric emptying

Animal Models for Functional Gastrointestinal Disorders

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