Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/7828
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dc.contributor.authorKostopoulos, G. K.en
dc.contributor.authorPsarropoulou, C. T.en
dc.date.accessioned2015-11-24T16:34:38Z-
dc.date.available2015-11-24T16:34:38Z-
dc.identifier.issn0300-9564-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/7828-
dc.rightsDefault Licence-
dc.subjectlong-term potentiationen
dc.subjectpyramidal cells-invitroen
dc.subjectrat hippocampal sliceen
dc.subjectd-aspartate receptorsen
dc.subjectextracellular potassiumen
dc.subjectdentate gyrusen
dc.subjectpostsynaptic excitabilityen
dc.subjectmediated inhibitionen
dc.subjectmembrane-propertiesen
dc.subjectsynaptic propertiesen
dc.titlePossible Mechanisms Underlying Hyperexcitability in the Epileptic Mutant Mouse Totteringen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondary<Go to ISI>://A1992JK96700009-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιώνel
heal.publicationDate1992-
heal.abstractTottering mice present a useful experimental model of genetically determined generalized epilepsy of the absence type. In electrophysiological recordings from hippocampal slices in vitro we found that the postsynaptic excitability (firing threshold) of pyramidal neurons in the CA1 area of tg/tg slices was significantly higher than that of normal slices. In spite of this hyperexcitability, in vitro epileptiform discharges were not observed spontaneously, or upon provocation by intracellular depolarizing pulses, or in response to moderate elevations (+2 mM) in extracellular potassium. The latter elevations actually induced significantly smaller increases in the CA1 synaptic responses of tg/tg as compared to normal slices. The hyperexcitability of tottering neurons could not be explained in terms of altered membrane electrical properties or any reduction of synaptic inhibition or increased capacity for long-term potentiation. Responses to noradrenaline, histamine and adenosine, as well as to the release of N-methyl-D-asparate channels - by eliminating Mg2+ - were comparable in tg/tg and normal slices. These studies show that hyperexcitability can be co-inherited with epilepsy and in this model its expression can be maintained in vitro. The neuronal mechanism of this expression remains elusive, as it does not appear to include some features known to be shared by experimental models of chemically or electrically induced epilepsy.en
heal.journalNameJournal of Neural Transmission-General Sectionen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

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