Changes in the cannabinoid (CB1) receptor expression level and G-protein activation in kainic acid induced seizures

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dc.contributor.authorBojnik, Engin
dc.contributor.authorTurunc, Ezgi
dc.contributor.authorArmagan, Guliz
dc.contributor.authorKanit, Lutfiye
dc.contributor.authorBenyhe, Sandor
dc.contributor.authorYalcin, Ayfer
dc.contributor.authorBorsodi, Anna
dc.date.accessioned2019-10-27T21:44:01Z
dc.date.available2019-10-27T21:44:01Z
dc.date.issued2012
dc.departmentEge Üniversitesien_US
dc.description.abstractIt has been known for centuries that exogenous cannabinoids, such as tetrahydrocannabinol have anticonvulsant activity. Recent studies have advanced our understanding of the endogenous cannabinoid system and renewed the interest in cannabinoids as a potential treatment for epilepsy. The endogenous cannabinoid system is rapidly activated after seizure activity but still little is known about the molecular mechanisms underlying the role of the cannabinoid system in epilepsy. In this study epileptiform activity was induced by kainic acid (KA) and effects of the CB1 receptor agonists N-(2-Chloroethyl)-5Z,8Z,11Z,14Z-eicosatetraenamide (ACEA) on G-protein signaling using the agonist-stimulated [S-35]GTP gamma S binding assay were evaluated. Control and KA treated rat hippocampus and cortex membranes were used. Our results showed that the ACEA displayed a high potency and efficacy in stimulating the G-proteins and when compared to the control animals, significant enhancements were observed in tissues from the KA treated animals. Potency and efficacy values were in particular increased in the hippocampus tissues. Furthermore, gene expression levels of the cannabinoid receptor 1 (CB1) receptor and cannabinoid receptor interacting protein 1 (CRIP1) were measured by RT-PCR, where both CB1 and CRIP1 expressions were found to be elevated in the KA treated animals. (C) 2011 Elsevier B.V. All rights reserved.en_US
dc.description.sponsorshipHungary ETT [398-03]; OTKAOrszagos Tudomanyos Kutatasi Alapprogramok (OTKA) [CK-78566]; Technological and Scientific Council of Turkey (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [SBAG-106S249]; TUBITAKTurkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK); [TUR-11/2006]en_US
dc.description.sponsorshipThis study was supported by grants from Hungary ETT 398-03, TUR-11/2006, OTKA (CK-78566) and from The Technological and Scientific Council of Turkey (TUBITAK) (SBAG-106S249 to A.Y.). G.A. and E.T. were also supported by doctoral grants from TUBITAK. The helpful suggestions of Mr. Brendan Doe (CNR-IBCN, Rome, Italy) is greatly acknowledged.en_US
dc.identifier.doi10.1016/j.eplepsyres.2011.10.020en_US
dc.identifier.endpage68en_US
dc.identifier.issn0920-1211
dc.identifier.issue01.Feben_US
dc.identifier.pmid22079489en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage64en_US
dc.identifier.urihttps://doi.org/10.1016/j.eplepsyres.2011.10.020
dc.identifier.urihttps://hdl.handle.net/11454/47184
dc.identifier.volume99en_US
dc.identifier.wosWOS:000302431700008en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Science Bven_US
dc.relation.ispartofEpilepsy Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCannabinoid receptoren_US
dc.subjectEpilepsyen_US
dc.subjectKainic aciden_US
dc.subjectG-protein activationen_US
dc.subjectACEAen_US
dc.titleChanges in the cannabinoid (CB1) receptor expression level and G-protein activation in kainic acid induced seizuresen_US
dc.typeArticleen_US

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