Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/24059
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dc.contributor.authorFerre, S.en
dc.contributor.authorCiruela, F.en
dc.contributor.authorBorycz, J.en
dc.contributor.authorSolinas, M.en
dc.contributor.authorQuarta, D.en
dc.contributor.authorAntoniou, K.en
dc.contributor.authorQuiroz, C.en
dc.contributor.authorJustinova, Z.en
dc.contributor.authorLluis, C.en
dc.contributor.authorFranco, R.en
dc.contributor.authorGoldberg, S. R.en
dc.date.accessioned2015-11-24T19:37:39Z-
dc.date.available2015-11-24T19:37:39Z-
dc.identifier.issn1093-9946-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24059-
dc.rightsDefault Licence-
dc.subjectcaffeineen
dc.subjectpsychostimulantsen
dc.subjectadenosine receptorsen
dc.subjectreceptor heteromersen
dc.subjectstriatumen
dc.subjectreviewen
dc.subjectreceptor-mediated modulationen
dc.subjectcotransfected fibroblast cellsen
dc.subjectdopamine d-1 receptorsen
dc.subjecta(2a) receptorsen
dc.subjecta(1) receptoren
dc.subjectnucleus-accumbensen
dc.subject6-hydroxydopamine-lesioned ratsen
dc.subjectsquirrel-monkeysen
dc.subjectmice lackingen
dc.subjectinvolvementen
dc.titleAdenosine A(1)-A(2A) receptor heteromers: new targets for caffeine in the brainen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primaryDoi 10.2741/2852-
heal.identifier.secondary<Go to ISI>://000255775700196-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2008-
heal.abstractThe contribution of blockade of adenosine A(1) and A(2A) receptor to the psychostimulant effects of caffeine is still a matter of debate. When analyzing motor activity in rats, acutely administered caffeine shows a profile of a nonselective adenosine receptor antagonist, although with preferential A(1) receptor antagonism. On the other hand, tolerance to the effects of A(1) receptor blockade seems to be mostly responsible for the tolerance to the motor-activating effects of caffeine, while the residual motor-activating effects of caffeine in tolerant individuals seem to involve A(2A) receptor blockade. These behavioral studies correlate with in vivo microdialysis experiments that suggest that A(1) receptor-mediated modulation of striatal glutamate release is involved in the psychostimulant effects of caffeine. Experiments in transfected cells demonstrate the ability of A(1) receptors to heteromerize with A(2A) receptors and the A(1)-A(2A) receptor heteromer can be biochemically identified in the striatum, in striatal glutamatergic terminals. The striatal A(1)-A(2A) receptor heteromer provides a "concentration-dependent switch" mechanism by which low and high concentrations of synaptic adenosine produce the opposite effects on glutamate release. The analysis of the function of A(1)-A(2A) receptor heteromers during chronic treatment with caffeine gives new clues about the well-known phenomenon of tolerance to the psychostimulant effects of caffeine.en
heal.journalNameFrontiers in Bioscience-Landmarken
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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