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      Peripheral and spinal 5-HT receptors participate in cholestatic itch and antinociception induced by bile duct ligation in rats

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          Abstract

          Although 5-HT has been implicated in cholestatic itch and antinociception, two common phenomena in patients with cholestatic disease, the roles of 5-HT receptor subtypes are unclear. Herein, we investigated the roles of 5-HT receptors in itch and antinociception associated with cholestasis, which was induced by common bile duct ligation (BDL) in rats. 5-HT-induced enhanced scratching and antinociception to mechanical and heat stimuli were demonstrated in BDL rats. 5-HT level in the skin and spinal cord was significantly increased in BDL rats. Quantitative RT-PCR analysis showed 5-HT 1B, 5-HT 1D, 5-HT 2A, 5-HT 3A, 5-HT 5B, 5-HT 6, and 5-HT 7 were up-regulated in peripheral nervous system and 5-HT 1A, 5-HT 1F, 5-HT 2B, and 5-HT 3A were down-regulated in the spinal cord of BDL rats. Intradermal 5-HT 2, 5-HT 3, and 5-HT 7 receptor agonists induced scratching in BDL rats, whereas 5-HT 3 agonist did not induce scratching in sham rats. 5-HT 1A, 5-HT 2, 5-HT 3, and 5-HT 7 agonists or antagonists suppressed itch in BDL rats. 5-HT 1A agonist attenuated, but 5-HT 1A antagonist enhanced antinociception in BDL rats. 5-HT 2 and 5-HT 3 agonists or antagonists attenuated antinociception in BDL rats. Our data suggested peripheral and central 5-HT system dynamically participated in itch and antinociception under cholestasis condition and targeting 5-HT receptors may be an effective treatment for cholestatic itch.

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          Descending control of pain.

          Mark J Millan (2002)
          Upon receipt in the dorsal horn (DH) of the spinal cord, nociceptive (pain-signalling) information from the viscera, skin and other organs is subject to extensive processing by a diversity of mechanisms, certain of which enhance, and certain of which inhibit, its transfer to higher centres. In this regard, a network of descending pathways projecting from cerebral structures to the DH plays a complex and crucial role. Specific centrifugal pathways either suppress (descending inhibition) or potentiate (descending facilitation) passage of nociceptive messages to the brain. Engagement of descending inhibition by the opioid analgesic, morphine, fulfils an important role in its pain-relieving properties, while induction of analgesia by the adrenergic agonist, clonidine, reflects actions at alpha(2)-adrenoceptors (alpha(2)-ARs) in the DH normally recruited by descending pathways. However, opioids and adrenergic agents exploit but a tiny fraction of the vast panoply of mechanisms now known to be involved in the induction and/or expression of descending controls. For example, no drug interfering with descending facilitation is currently available for clinical use. The present review focuses on: (1) the organisation of descending pathways and their pathophysiological significance; (2) the role of individual transmitters and specific receptor types in the modulation and expression of mechanisms of descending inhibition and facilitation and (3) the advantages and limitations of established and innovative analgesic strategies which act by manipulation of descending controls. Knowledge of descending pathways has increased exponentially in recent years, so this is an opportune moment to survey their operation and therapeutic relevance to the improved management of pain.
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            A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia.

            Mark Brown, Sonia Flores, R Dubner … (1987)
            A method to measure cutaneous hyperalgesia to thermal stimulation in unrestrained animals is described. The testing paradigm uses an automated detection of the behavioral end-point; repeated testing does not contribute to the development of the observed hyperalgesia. Carrageenan-induced inflammation resulted in significantly shorter paw withdrawal latencies as compared to saline-treated paws and these latency changes corresponded to a decreased thermal nociceptive threshold. Both the thermal method and the Randall-Selitto mechanical method detected dose-related hyperalgesia and its blockade by either morphine or indomethacin. However, the thermal method showed greater bioassay sensitivity and allowed for the measurement of other behavioral parameters in addition to the nociceptive threshold.
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              TRPA1 is required for histamine-independent, Mas-related G protein-coupled receptor-mediated itch

              Sarah R Wilson, Kristin A. Gerhold, Amber Bifolck-Fisher … (2011)
              SUMMARY Itch, the unpleasant sensation that evokes a desire to scratch, accompanies numerous skin and nervous system disorders. In many cases, pathological itch is insensitive to antihistamine treatment. Recent studies have identified members of the Mas-related GPCR (Mrgpr) family that are activated by mast cell mediators and promote histamine-independent itch. MrgprA3 and MrgprC11 act as receptors for the pruritogens chloroquine and BAM8–22, respectively. However, the signaling pathways and transduction channels activated downstream of these pruritogens are largely unknown. We found that TRPA1 is the downstream target of both MrgprA3 and MrgprC11, in cultured sensory neurons and heterologous cells. TRPA1 is required for Mrgpr-mediated signaling, as sensory neurons from TRPA1-deficient mice exhibited profoundly diminished responses to chloroquine and BAM8–22. Likewise, TRPA1-deficient mice displayed little to no scratching in response to these pruritogens. Our findings demonstrate that TRPA1 is an essential component of the signaling pathways that promote histamine-independent itch.
              Article 0 comments Cited 189 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 08 November 2016
                Publication date Collection: 2016
                Volume: 6
                Electronic Location Identifier: 36286
                Affiliations
                [1 ]Department of General Surgery, The Second Affiliated Hospital of Soochow University , Suzhou, 215004, China
                [2 ]Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, Soochow University , Suzhou, Jiangsu, 215123, China
                [3 ]Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, School of Public Health, Soochow University , Suzhou, 215123, China
                [4 ]Department of Anesthesiology, The First Affiliated Hospital of Soochow University , Suzhou, 215006, China
                Author notes
                [†]

                Present address: Capital Medical University Electric Power Teaching Hospital, Beijing, 100073, China.

                [*]

                These authors contributed equally to this work.

                Article
                Publisher Item ID: srep36286
                DOI: 10.1038/srep36286
                PMC ID: 5099756
                PubMed ID: 27824106
                SO-VID: ba014e33-1655-4e7e-8acb-39d3880081d0
                Copyright © Copyright © 2016, The Author(s)
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 13 June 2016
                Date accepted : 13 October 2016
                Categories
                Subject: Article

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