Peripheral corticotropin-releasing factor and stress-stimulated colonic motor activity involve type 1 receptor in rats

Maillot, C; Million, Mulugeta; Wei, Jiann-Wu; Gauthier, Ariane; Taché, Yvette

doi:10.1053/gast.2000.20251

Cited by 189 publications

(272 citation statements)

References 37 publications

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“…A genetic variation in intestinal stress response has also been documented in other rat strains, e.g., Fischer and Lewis rats (18). In this study, we sought to determine whether neonatal stress, which causes phenotypic changes in behavior and systemic parameters, also affects the sensitivity to stress-induced functional changes of the colonic mucosa in genetically stressresistant Sprague-Dawley rats.…”

Section: Discussionmentioning

confidence: 96%

“…The involvement of neurons was suggested by modulation of the CRH response by atropine, hexamethonim, and bretylium (5,28). Peripheral effects of CRH have been shown to regulate colonic motor activity (18), and expression of CRH and CRH receptors is also found in the colonic mucosa of rodents (19) and humans (13,23). Coutinho et al (7) recently reported that maternal separation induced visceral hyperalgesia and increased colonic motility in adult rats.…”

Section: Discussionmentioning

confidence: 99%

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Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress

Söderholm¹,

Yates²,

Gareau³

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

207

208

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. Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress. Am J Physiol Gastrointest Liver Physiol 283: G1257-G1263, 2002. First published August 28, 2002 10.1152/ajpgi.00314.2002Intestinal dysfunction is related to stress and early life events, but the mechanisms are largely unknown. Our aim was to determine whether early trauma predisposes adult rats to intestinal mucosal dysfunction in response to stress. Neonatal Sprague-Dawley rats were individually separated from their mothers for 3 h/day at 4-21 days of age. Between days 80 and 90, separated and control rats were subjected to mild acute stress (30-min water avoidance) or sham stress. Mucosal barrier function and ion transport were assessed in colonic tissues mounted in Ussing chambers. Mild stress increased short-circuit current, conductance, and transepithelial transport of macromolecules in separated rats, while having minimal effects in controls. Pretreatment of the separated rats with a corticotropin-releasing hormone (CRH) antagonist, the peptide ␣-helical CRH(9-41) injected intraperitoneally 20 min before stress, abolished the stress-induced mucosal changes. Our results indicate that neonatal trauma can induce phenotypic changes in adulthood, including enhanced vulnerability of the gut mucosa to stress via mechanisms involving peripherally located CRH receptors.behavior; corticotropin-releasing hormone; electron microscopy; ion transport; intestinal permeability HUMANS EXPERIENCE STRESS OF various types during daily life, and adequate responses to these stressors are necessary for survival. If the severity or the chronicity of the stressful experience exceeds the adaptive capacity, the individual will be predisposed to illness and disease in multiple organ systems (21). A large number of studies have shown that early-life experience plays an important role in stress responsiveness throughout life (8). In animal models, neonatal adversity can result in permanent functional changes in the stress-mediating systems of the central nervous system (15). For example, newborn rats subjected to maternal separation demonstrate increased release of corticotropinreleasing hormone (CRH), altered expression of glucocorticoid receptors, as well as changes in the norepinephrine and GABA systems (3, 4). Recently, it was also shown in humans that adverse early-life events are associated with hyperresponsiveness to stress and alterations in the hypothalamic-pituitaryadrenal (HPA) axis (10).There is evidence that early-life trauma and ongoing psychological stress can affect the clinical course of intestinal disorders (16,17,20,26) and also reactivate inflammation in experimental colitis (6,9,22,25). The mechanisms underlying stress-induced exacerbations of intestinal diseases are, however, largely unknown. One possible link between intestinal disease and stress is a change in mucosal function. Our previous studies have shown that acute stress in rats induces enhanced intestinal epithelial permeability to macromolecu...

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress

Söderholm¹,

Yates²,

Gareau³

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

207

208

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“…Stress can have differential effects on gastrointestinal motor responses -delaying gastric emptying while simultaneously accelerating large bowel transit, and there are numerous reports, both clinical and experimental, implicating stress as a significant modulator of gastrointestinal motor function [22]. Since defecation responses are a reliable measure of autonomic nervous system modulation of colonic motility, fecal pellet output was recorded to see if the stress paradigm utilized in the present study affected gastrointestinal motor function in high-and/or low-anxiety rats.…”

Section: Discussionmentioning

confidence: 99%

Chronic psychological stress enhances nociceptive processing in the urinary bladder in high-anxiety rats

Robbins

DeBerry

Ness

2007

Physiology & Behavior

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This study sought to determine whether acute and/or chronic psychological stress produce changes in urinary bladder nociception. Female Sprague-Dawley (SD; low/moderate anxiety) or WistarKyoto (WK; high-anxiety) rats were exposed to either an acute (1 day) or a chronic (10 days) water avoidance stress paradigm or a sham stress paradigm. Paw withdrawal thresholds to mechanical and thermal stimuli and fecal pellet output, were quantified at baseline and after the final stress or sham stress exposure. Rats were then sedated, and visceromotor responses (VMRs) to urinary bladder distension (UBD) were recorded. While acute stress exposure did not significantly alter bladder nociceptive responses in either strain of rats, WK rats exposed to a chronic stress paradigm exhibited enhanced responses to UBD. These high-anxiety rats also exhibited somatic analgesia following acute, but not chronic, stress. Furthermore, WK rats had greater fecal pellet output than SD rats when stressed. Significant stress-induced changes in nociceptive responses to mechanical stimuli were observed in SD rats. That chronic psychological stress significantly enhanced bladder nociceptive responses only in high-anxiety rats provides further support for a critical role of genetics, stress and anxiety as exacerbating factors in painful urogenital disorders such as interstitial cystitis (IC).

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“…14 Of the two CRF receptor subtypes, CRF-R1 stimulates colonic motility and defecation, whereas CRF-R2 inhibits gastric emptying and gastric contraction at times of stress. 15 Anatomical, physiological, pharmacological and biochemical studies have provided unambiguous evidence that the CRF system (CRF, urocortins, CRF-R1 and CRF-R2) is the key player of gastrointestinal motility disturbance during times of stress. 7,16 Hypothesis: in utero meconium passage is a fetal neurovisceral motor response to stress We hypothesize that in utero meconium passage is a neurovisceral motor response to fetal stress and that the CRF system plays a critical role in the stimulation of cholinergically mediated fetal colonic propulsive motor functions that trigger meconium passage.…”

Section: Introductionmentioning

confidence: 99%

“…Ongoing studies in our laboratory also support the expression of CRF-R1 in smooth muscle and enteric neuronal circuitry in term rat fetal gastrointestinal tract, 26 lending strong anatomical support for our hypothesis that intrauterine stress may impact gut motility through CRF-R1 in a manner analogous to stress-induced stimulation of colonic motility and defecation in adult rats. 15 Lessons learned from sheep model in support of stress-induced in utero meconium passage Sheep are used in our laboratory as a large animal model for understanding the molecular mechanism of in utero meconium passage. [27][28][29] The larger size of the gut and longer gestational age permit in vivo studies exploring gestation-and hormone-dependent changes in gastrointestinal motility, and in vitro organ bath studies examining smooth muscle contractility.…”

Section: Introductionmentioning

confidence: 99%

Mechanism(s) of in utero meconium passage

Lakshmanan

Ross

2008

J Perinatol

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To use sheep and rat models and demonstrate that stressors activate fetal glucocorticoid (GC) system, corticotrophin-releasing factor (CRF) system and cholinergic neurotransmitter system (ChNS) leading to propulsive colonic motility and in utero meconium passage. Immunohistochemical studies (IHS) were performed to localize GC-Receptors, CRF-receptors and key molecules of ChNS in sheep fetal distal colon. CRF expression in placenta and enteric endocrine cells in fetal rat system were examined and the effects of acute hypoxia on in utero meconium passage was tested. IHS confirmed localization and gestation dependent changes in GC-Rs, CRF-Rs and cholinergic markers in sheep fetal colon. Rat placenta and enteric endocrine cells express CRF and gastrointestinal tract express CRF-Rs. Hypoxia is a potent inducer of meconium passage in term fetal rats. Stress is a risk factor for in utero meconium passage and laboratory animal models can be used to develop pharmacotherapy to prevent stress-induced in utero meconium passage.

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Peripheral corticotropin-releasing factor and stress-stimulated colonic motor activity involve type 1 receptor in rats

Cited by 189 publications

References 37 publications

Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress

Neonatal maternal separation predisposes adult rats to colonic barrier dysfunction in response to mild stress

Chronic psychological stress enhances nociceptive processing in the urinary bladder in high-anxiety rats

Mechanism(s) of in utero meconium passage

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