Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/20855
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dc.contributor.authorPelidou, S. H.en
dc.contributor.authorSchultzberg, M.en
dc.contributor.authorIverfeldt, K.en
dc.date.accessioned2015-11-24T19:10:41Z-
dc.date.available2015-11-24T19:10:41Z-
dc.identifier.issn0165-5728-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20855-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectCell Death/drug effects/immunologyen
dc.subjectCell Survival/drug effects/immunologyen
dc.subjectCerebellar Cortex/drug effects/immunology/*metabolismen
dc.subjectEncephalitis/genetics/immunology/metabolismen
dc.subjectExcitatory Amino Acid Antagonists/pharmacologyen
dc.subjectGlutamic Acid/*pharmacologyen
dc.subjectMiceen
dc.subjectMice, Knockouten
dc.subjectNeurodegenerative Diseases/genetics/immunology/metabolismen
dc.subjectNeurons/drug effects/immunology/*metabolismen
dc.subjectNeurotoxins/*pharmacologyen
dc.subjectReceptors, Interleukin-1/*deficiency/geneticsen
dc.subjectReceptors, Interleukin-1 Type Ien
dc.subjectReceptors, N-Methyl-D-Aspartate/drug effects/*metabolismen
dc.titleIncreased sensitivity to N-methyl-D-aspartate receptor-induced excitotoxicity in cerebellar granule cells from interleukin-1 receptor type I-deficient miceen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/12446013-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2002-
heal.abstractThe effects of chronic exposure to excitatory amino acids (EAAs) were examined in cultured cerebellar granule cells (CGCs) from wild type (WT) and interleukin-1 receptor type I (IL-1RI)-deficient mice. After 8 days in culture, the cells were exposed to 100 microM glutamate or 300 microM N-methyl-D-aspartate (NMDA) for 24 h. Analysis of cell viability, as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction assay and phase-contrast microscopy revealed that CGCs from IL-1RI-deficient mice were more vulnerable to EAAs as compared to the WT controls. The results indicate that IL-1RI signalling is important for neuronal survival. The effect of glutamate on the CGCs from IL-1RI-deficient mice was decreased by the non-competitive NMDA-receptor antagonist MK-801, supporting the involvement of NMDA receptors in the glutamate-induced excitotoxicity.en
heal.journalNameJ Neuroimmunolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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