Corticotropin-releasing factor induces rectal hypersensitivity after repetitive painful rectal distention in healthy humans

Nozu, Tsukasa; Kudaira, Miwako

doi:10.1007/s00535-006-1848-4

Cited by 42 publications

(32 citation statements)

References 17 publications

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“…In light of the recent increasing interest in the potential modulating effects of CRF in clinically relevant pain conditions such as visceral pain (Nozu and Kudaira, 2006;Sagami et al, 2004), postoperative joint pain (Likar et al, 2007), and fibromyalgia (McLean et al, 2006;Lund et al, 2006), we set out to investigate systematically the antinociceptive effects of CRF at the three main levels of the neuraxis of pain transmission, that is, at the level of the brain, spinal cord, and periphery. As it was suggested that antinociceptive effects of CRF are identified rather in tonic than in phasic pain (Lariviere and Melzack, 2000), we have chosen an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Mousa

Bopaiah

Richter

et al. 2007

Neuropsychopharmacol

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There is conflicting evidence on the antinociceptive effects of corticotropin-releasing factor (CRF) along the neuraxis of pain transmission and the responsible anatomical sites of CRF's action at the level of the brain, spinal cord and periphery. In an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation, we systematically investigated CRF's ability to modulate inflammatory pain at those three levels of pain transmission by algesiometry following the intracerebroventricular, intrathecal, and intraplantar application of low, systemically inactive doses of CRF. At each level, CRF elicits potent antinociceptive effects, which are dose dependent and antagonized by local, but not systemic CRF receptor antagonist a-helical CRF indicating CRF receptor specificity. Consistently, we have identified by immunohistochemistry multiple brain areas, inhibitory interneurons within the dorsal horn of the spinal cord as well as immune cells within subcutaneous tissueFbut not peripheral sensory neuronsFthat coexpress both CRF receptors and opioid peptides. In line with these anatomical findings, local administration of CRF together with the opioid receptor antagonist naloxone dosedependently reversed CRF's antinociceptive effects at each of these three levels of pain transmission. Therefore, local application of low, systemically inactive doses of CRF at the level of the brain, spinal cord and periphery inhibits tonic inflammatory pain most likely through an activation of CRF receptors on cells that coexpress opioid peptides which results in opioid-mediated pain inhibition. Future studies have to delineate whether endogenous CRF at these three levels contributes to the body's response to cope with the stressful stimulus pain in an opioid-mediated manner.

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Section: Introductionmentioning

confidence: 99%

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Mousa

Bopaiah

Richter

et al. 2007

Neuropsychopharmacol

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“…One study demonstrated a greater increase in perception of colonic distension after intravenous CRH administration in healthy individuals, in contrast to the response prior to administration or following placebo. 18 Another study reported that when a-helical CRH was peripherally administered in IBS patients, the hyperresponsiveness to stress induced by colonic electrical stimulation was suppressed. 8 These results indicate that stress is closely associated with colonic perception and bowel movements.…”

Section: Discussionmentioning

confidence: 99%

Intravenous Corticotropin-releasing Hormone Administration Increases Esophageal Electrical Sensitivity in Healthy Individuals

Yamasaki

Tomita

Takimoto

et al. 2017

J Neurogastroenterol Motil

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Background/AimsWhen a person is experiencing stress, corticotropin-releasing hormone (CRH) can modulate gut physiologies, such as visceral sensation or gastrointestinal motility, and its intravenous administration mimics stress-induced physiological changes. However, the influence of CRH on the esophagus is yet unknown. Accordingly, we investigated whether intravenous CRH administration increases esophageal sensitivity to electrical stimulation in healthy Japanese subjects. MethodsTwenty healthy subjects were recruited. We quantified the initial perception threshold (IPT) every 15 minutes after CRH injection. Venous blood was collected with a cannula, and both plasma adrenocorticotropic hormone (ACTH) and cortisol were measured at pre-stimulation, 0, 30, 60, 90, and 120 minutes. The results from each time point were compared against a baseline IPT obtained before electrical stimulation was initiated. ResultsWhen compared to the baseline IPT value (16.9 ± 4.5), CRH significantly decreased electrical threshold of the esophagus at 30, 45, 60, 75 minutes (14.1 ± 4.2, 13.1 ± 5.0, 12.1 ± 5.7, 14.0 ± 5.8 minutes, P < 0.01, respectively) after CRH injection, suggesting that CRH increased esophageal sensitivity to the electrical stimulus. CRH also significantly increased plasma ACTH levels at 30 minutes (50.3 ± 17.7, P < 0.01), and cortisol levels at 30 minutes (22.0 ± 6.7 minutes, P < 0.01) and 60 minutes (20.3 ± 6.7 minutes, P < 0.01) after CRH injection, when compared to the pre-stimulation ACTH and cortisol values. ConclusionIntravenous CRH administration increased esophageal electrical sensitivity in normal subjects, emphasizing the important role of stress in esophageal sensitivity.

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“…An alteration in central noradrenergic signaling is observed in IBS; early life trauma may be one mediator of these abnormalities [ 20 ]. In healthy controls, CRF iv decreases rectal pain threshold to distension and mimics an IBS-specifi c visceral response [ 137 ]. Peripheral injection of α-helical CRF9 − 41 prevents rectal electrical stimulation-induced enhanced sigmoid colonic motility, visceral perception, and anxiety in IBS patients compared to controls without altering the HPA axis [ 161 ] and improves decreased alpha power spectra and increases beta power spectra of electroencephalogram in IBS patients [ 190 ].…”

Section: Implication In Functional Digestive Disorders and Infl Ammatmentioning

confidence: 98%

Stress and the Gastrointestinal System

Bonaz

2016

Neuro-Immuno-Gastroenterology

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Stress was characterized by Hans Selye, in 1936, as the "stereotyped biological response to any demand." Corticotrophin-releasing factor (CRF) and its related peptides urocortins (Ucns 1,2,3) are the mediators of stress. They are present both in the central nervous system and in the gastrointestinal (GI) tract where they exert their biological actions on target cells through activation of two receptors, CRF1 and CRF2. Stress is able to modulate numerous functions of the GI tract such as motility, secretion, permeability, sensitivity, and microbiota. Classically, stress delays gastric emptying while stimulating colonic transit and secretion, increases intestinal permeability and visceral sensitivity, and modifi es intestinal microbiota. Through these various effects at the level of the GI tract, stress is involved in the pathophysiology of irritable bowel syndrome (IBS), a functional digestive disorder, as well as infl ammatory bowel disease (IBD), Crohn's disease, and ulcerative colitis. Targeting these CRF1/CRF2 signaling pathways by selective antagonists/agonists should be of clinical interest in the domain of IBS and IBD. Stress-Defi nitionIn 1936, Hans Selye defi ned the concept of stress as the "stereotyped biological response to any demand" [ 168 ] and elaborated the concept of the general adaptation syndrome. Later, the hypothalamic factor named corticotrophin-releasing factor (CRF) which stimulates ACTH release by the rat pituitary was discovered [ 77 ], positioning the hypothalamic-pituitary adrenal (HPA) axis as a key element in this concept. In 1981, Vale and his group [ 196 ] identifi ed the 41-aa peptide CRF characterized

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Corticotropin-releasing factor induces rectal hypersensitivity after repetitive painful rectal distention in healthy humans

Abstract: These results indicate that CRF modifies rectal sensation in healthy humans and mimics an IBS-specific visceral response, suggesting the possible contribution of CRF to the pathogenesis of IBS.

Cited by 42 publications

References 17 publications

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Intravenous Corticotropin-releasing Hormone Administration Increases Esophageal Electrical Sensitivity in Healthy Individuals

Stress and the Gastrointestinal System

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