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DC Field | Value | Language |
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dc.contributor.author | Laudadio, M. A. | en |
dc.contributor.author | Psarropoulou, C. | en |
dc.date.accessioned | 2015-11-24T16:33:20Z | - |
dc.date.available | 2015-11-24T16:33:20Z | - |
dc.identifier.issn | 0920-1211 | - |
dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/7648 | - |
dc.rights | Default Licence | - |
dc.subject | purinergic | en |
dc.subject | development | en |
dc.subject | adenosine receptors | en |
dc.subject | electrophysiology | en |
dc.subject | extracellular recordings | en |
dc.subject | synchronous potentials | en |
dc.subject | rat | en |
dc.subject | induced epileptogenesis | en |
dc.subject | cerebral-ischemia | en |
dc.subject | a(2) receptors | en |
dc.subject | uptake sites | en |
dc.subject | in-vitro | en |
dc.subject | ca3 area | en |
dc.subject | brain | en |
dc.subject | activation | en |
dc.subject | modulation | en |
dc.subject | blockade | en |
dc.title | The A(3) adenosine receptor agonist 2-Cl-IB-MECA facilitates epileptiform discharges in the CA(3) area of immature rat hippocampal slices | en |
heal.type | journalArticle | - |
heal.type.en | Journal article | en |
heal.type.el | Άρθρο Περιοδικού | el |
heal.identifier.primary | DOI 10.1016/j.eplepsyres.2004.03.005 | - |
heal.identifier.secondary | <Go to ISI>://000222964000002 | - |
heal.identifier.secondary | http://ac.els-cdn.com/S0920121104000488/1-s2.0-S0920121104000488-main.pdf?_tid=afd0d808-ad80-11e2-9454-00000aab0f27&acdnat=1366878079_c5d473feabed8e7ebefb129a46dceb97 | - |
heal.language | en | - |
heal.access | campus | - |
heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιών | el |
heal.publicationDate | 2004 | - |
heal.abstract | The 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.journalName | Epilepsy Res | en |
heal.journalType | peer reviewed | - |
heal.fullTextAvailability | TRUE | - |
Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) |
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Psarropoulou-2004-The A3 adenosine.pdf | 214.57 kB | Adobe PDF | View/Open Request a copy |
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