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dc.contributor.authorLaudadio, M. A.en
dc.contributor.authorPsarropoulou, C.en
dc.date.accessioned2015-11-24T16:33:20Z-
dc.date.available2015-11-24T16:33:20Z-
dc.identifier.issn0920-1211-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/7648-
dc.rightsDefault Licence-
dc.subjectpurinergicen
dc.subjectdevelopmenten
dc.subjectadenosine receptorsen
dc.subjectelectrophysiologyen
dc.subjectextracellular recordingsen
dc.subjectsynchronous potentialsen
dc.subjectraten
dc.subjectinduced epileptogenesisen
dc.subjectcerebral-ischemiaen
dc.subjecta(2) receptorsen
dc.subjectuptake sitesen
dc.subjectin-vitroen
dc.subjectca3 areaen
dc.subjectbrainen
dc.subjectactivationen
dc.subjectmodulationen
dc.subjectblockadeen
dc.titleThe A(3) adenosine receptor agonist 2-Cl-IB-MECA facilitates epileptiform discharges in the CA(3) area of immature rat hippocampal slicesen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primaryDOI 10.1016/j.eplepsyres.2004.03.005-
heal.identifier.secondary<Go to ISI>://000222964000002-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0920121104000488/1-s2.0-S0920121104000488-main.pdf?_tid=afd0d808-ad80-11e2-9454-00000aab0f27&acdnat=1366878079_c5d473feabed8e7ebefb129a46dceb97-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιώνel
heal.publicationDate2004-
heal.abstractThe effects of the A(3) adenosine receptor agonist 2-Cl-IB-MECA were tested on epileptiform field potentials recorded in the CA3 area of postnatal days 10-20 immature hippocampal slices, during perfusion with the GABA(A) receptor antagonist bicuculline (10 muM). Evoked potentials: 2-Cl-IB-MECA (1-50 muM, n = 17) had consistently excitatory effects, blocked by the A3 receptor antagonist MRS 1220 (1 muM, n = 7), but not occluded in the presence of the A(1) antagonist DPCPX (1 muM, n = 12) or the A(2A) antagonist ZM-241385 (0.1 muM, n = 12). 2-Cl-IB-MECA reversed the inhibitory effects (n = 5) of the adenosine uptake blocker nitrobenzylthioinosine (NBTI, 50 muM), but did not increase its excitatory effects (n = 19). Spontaneous discharges: 2-Cl-113-MECA (1 muM) induced them or increased their frequency in 14/30 slices, an effect reversed by MRS 1220 (n = 3), and observed also following pre-perfusion with DPCPX (n = 11), ZM-241385 (n = 11) or both (n = 10). In the presence of the A(1) antagonist DPCPX, NBTI increased the frequency of spontaneous discharges, an effect partially reversed by MRS 1220 (n = 8), thus suggesting that a rise in endogenous adenosine during disinhibition may activate A3 receptors. In conclusion, these findings suggest strongly that activation of A3 receptors, following a rise in endogenous adenosine (i.e. during seizures, hypoxia), facilitates excitation, thus limiting the known inhibitory and/or neuroprotective effects of adenosine in immature brain. (C) 2004 Elsevier B.V. All rights reserved.en
heal.journalNameEpilepsy Resen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
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