Attenuation of serotonin-induced itch responses by inhibition of endocannabinoid degradative enzymes, fatty acid amide hydrolase and monoacylglycerol lipase

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dc.authoridGunduz, Ozgur/0000-0002-2470-3021
dc.authoridUlugol, Ahmet/0000-0003-4643-1124;
dc.authorwosidGunduz, Ozgur/A-2351-2016
dc.authorwosidUlugol, Ahmet/V-9665-2019
dc.authorwosidGÜNDÜZ, Özgür/AAH-8717-2019
dc.contributor.authorTosun, Nurcan Calimli
dc.contributor.authorGunduz, Ozgur
dc.contributor.authorUlugol, Ahmet
dc.date.accessioned2024-06-12T10:51:21Z
dc.date.available2024-06-12T10:51:21Z
dc.date.issued2015
dc.departmentTrakya Üniversitesien_US
dc.description.abstractItch and pain are two irritating sensations sharing a lot in common. Considering the antinociceptive effects of blockade of endocannabinoid degrading enzymes in pain states, we attempted to reduce scratching behavior by endocannabinoid modulation, i.e. by inhibiting fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL), or cellular uptake of endocannabinoids. Scratching behavior was induced by intradermal injection of serotonin to Balb/c mice. URB597 (10 mg/kg, i.p.), a FAAH inhibitor, JZL184 (16 mg/kg, i.p.), a MAGL inhibitor, and AM404 (10 mg/kg, i.p.), an endocannabinoid transport inhibitor, were given to evaluate the effects of endocannabinoid modulation on scratching responses. Then, the CB1 receptor antagonist, AM251 (1 mg/kg, i.p.), and the CB2 receptor antagonist, SR144528 (1 mg/kg, i.p.), were administered to determine whether cannabinoid receptors mediate these effects. URB597 and JZL184, but not AM404, attenuated serotonin-induced scratches. The inhibitory effect of URB597 was reversed by SR144528, but cannabinoid receptor antagonists had no other effects on modulation by the inhibitors. We propose that augmenting the endocannabinoid tonus by inhibition of degradative enzymes, FAAH and MAGL, but not cellular uptake, may be a novel target for the development of antipruritic agents.en_US
dc.description.sponsorshipTrakya University Research Council [TUBAP-2012/187]en_US
dc.description.sponsorshipThis work was supported by a grant from Trakya University Research Council (TUBAP-2012/187). The authors have no conflicts of interests to report.en_US
dc.identifier.doi10.1007/s00702-014-1251-x
dc.identifier.endpage367en_US
dc.identifier.issn0300-9564
dc.identifier.issn1435-1463
dc.identifier.issue3en_US
dc.identifier.pmid24915981en_US
dc.identifier.scopus2-s2.0-84939885953en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage363en_US
dc.identifier.urihttps://doi.org/10.1007/s00702-014-1251-x
dc.identifier.urihttps://hdl.handle.net/20.500.14551/18337
dc.identifier.volume122en_US
dc.identifier.wosWOS:000350033100004en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringer Wienen_US
dc.relation.ispartofJournal Of Neural Transmissionen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAM404en_US
dc.subjectEndocannabinoidsen_US
dc.subjectFAAHen_US
dc.subjectMAGLen_US
dc.subjectPruritusen_US
dc.subjectJZL184en_US
dc.subjectURB597en_US
dc.subjectCannabinoid Agonisten_US
dc.subjectInflammatory Painen_US
dc.subjectNeuropathic Painen_US
dc.subjectSpinal-Corden_US
dc.subjectMiceen_US
dc.subjectReceptorsen_US
dc.subjectSystemen_US
dc.subjectPruritusen_US
dc.subjectTargeten_US
dc.subjectFaahen_US
dc.titleAttenuation of serotonin-induced itch responses by inhibition of endocannabinoid degradative enzymes, fatty acid amide hydrolase and monoacylglycerol lipaseen_US
dc.typeArticleen_US

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