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Inflammopharmacology

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05.02.2018 | Review

The peripheral corticotropin-releasing factor (CRF)-induced analgesic effect on somatic pain sensitivity in conscious rats: involving CRF, opioid and glucocorticoid receptors

verfasst von: Natalia I. Yarushkina, Ludmila P. Filaretova

Erschienen in: Inflammopharmacology | Ausgabe 2/2018

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Abstract

The corticotropin-releasing factor (CRF) is involved in somatic pain regulation and may produce an analgesic effect in humans and animals, although the mechanisms of the CRF-induced analgesia remain unclear. CRF action is mediated by the CRF receptors of subtypes 1 and 2 (CRF-R1 and CRF-R2, respectively). Activation of the hypothalamic –pituitary –adrenocortical axis (HPA) is provided by CRF-R1; but CRF-R2 are also involved in the regulation of the HPA axis, and, respectively, glucocorticoids, the end hormones of the HPA axis, also participate in somatic pain regulation. Additionally, opioids may contribute to the CRF-induced analgesia. This article serves as an overview of the role of CRF-R1 and CRF-R2, as well as glucocorticoid and opioid receptors in peripheral CRF-induced analgesia in conscious rats, while we focused on the data obtained under normal (non-pathological) conditions including results of our studies in rats. The involvement of CRF-R1 and CRF-R2, glucocorticoids and opioid receptors was studied under the same experimental conditions following pretreatment with appropriate antagonists: NBI 27914, astressin₂-B, naltrexone and RU 38486, respectively. Somatic pain sensitivity was measured by the tail flick latencies induced by thermal stimulus (tail flick test). Peripheral administration of the CRF caused both an increase in the tail flick latencies (analgesic effect) and plasma corticosterone levels. Pretreatment with NBI 27914, astressin₂-B, naltrexone or RU 38486 attenuated the peripheral CRF-induced analgesia. The results obtained suggest that the peripheral CRF-induced analgesic effect may be mediated through the involvement of CRF-R1 and CRF-R2 as well as opioid and glucocorticoid receptors, including CRF-R2 and opioid receptors within periaqueductal gray matter of the midbrain.

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Titel: The peripheral corticotropin-releasing factor (CRF)-induced analgesic effect on somatic pain sensitivity in conscious rats: involving CRF, opioid and glucocorticoid receptors
verfasst von: Natalia I. Yarushkina
Ludmila P. Filaretova
Publikationsdatum: 05.02.2018
Verlag: Springer International Publishing
Erschienen in: Inflammopharmacology / Ausgabe 2/2018
Print ISSN: 0925-4692
Elektronische ISSN: 1568-5608
DOI: https://doi.org/10.1007/s10787-018-0445-5

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The peripheral corticotropin-releasing factor (CRF)-induced analgesic effect on somatic pain sensitivity in conscious rats: involving CRF, opioid and glucocorticoid receptors

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Protective effect of gallic acid in experimental model of ketamine-induced psychosis: possible behaviour, biochemical, neurochemical and cellular alterations

Terminalia arjuna prevents Interleukin-18-induced atherosclerosis via modulation of NF-κB/PPAR-γ-mediated pathway in Apo E−/− mice

Caffeic acid phenethyl ester is protective in experimental ulcerative colitis via reduction in levels of pro-inflammatory mediators and enhancement of epithelial barrier function

Carbon monoxide-releasing molecule, CORM-3, modulates alveolar macrophage M1/M2 phenotype in vitro

Molecular signature of nitric oxide on major cancer hallmarks of colorectal carcinoma

Downregulation of iNOS and elevation of cAMP mediate the anti-inflammatory effect of glabridin in rats with ulcerative colitis