Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/7481
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dc.contributor.authorLabrakakis, C.en
dc.contributor.authorMuller, T.en
dc.contributor.authorSchmidt, K.en
dc.contributor.authorKettenmann, H.en
dc.date.accessioned2015-11-24T16:31:47Z-
dc.date.available2015-11-24T16:31:47Z-
dc.identifier.issn0306-4522-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/7481-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectBarium/pharmacologyen
dc.subjectBicuculline/*pharmacologyen
dc.subjectCells, Cultureden
dc.subjectCerebellum/cytology/drug effects/*physiologyen
dc.subjectChloride Channels/*physiologyen
dc.subjectChlorides/*metabolismen
dc.subjectMembrane Potentials/drug effectsen
dc.subjectMiceen
dc.subjectMice, Inbred Strainsen
dc.subjectMuscimol/*pharmacen
dc.titleGABA(A) receptor activation triggers a Cl- conductance increase and a K+ channel blockade in cerebellar granule cellsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/9178874-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0306452296006446/1-s2.0-S0306452296006446-main.pdf?_tid=2944657a-c388-11e2-8c15-00000aab0f26&acdnat=1369300215_e5b84bc74faaa5e6d6f4b296ec32507e-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιώνel
heal.publicationDate1997-
heal.abstractGABA(A) receptor activation in cerebellar granule cells induced a complex physiological response, namely the activation of a Cl- conductance in concert with a blockade of the resting K+ outward conductance (by 71% as compared to controls). Both responses were mediated by the activation of GABA(A) receptors, since they were both mimicked by the GABA(A) receptor agonist muscimol and antagonized by picrotoxin and bicuculline. A substantial decrease of the mean open time of single, outwardly rectifying K+ channels was triggered by GABA as revealed from cell-attached recordings; this finding implies that an intracellular pathway links GABA(A) receptors and K+ channels. Furthermore, this action of GABA is mediated through the cytoplasm, as experiments with the cell-attached patch-clamp technique show. GABA induced a prominent membrane depolarization ranging from 10 to 25 mV as revealed by current-clamp recordings of gramicidin (or nystatin) permeabilized patches, thus selecting conditions not to perturb the physiological Cl- gradient across the cell. Our findings imply that the GABA-activated Cl- current depolarized the membrane as described for immature neurons. The blockade of the resting K+ channel conductance acts in concert and both mechanisms lead to this substantial depolarizing event.en
heal.journalNameNeuroscienceen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

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