Increased sensitivity to N-methyl-D-aspartate receptor-induced excitotoxicity in cerebellar granule cells from interleukin-1 receptor type I-deficient mice
| dc.contributor.author | Pelidou, S. H. | en |
| dc.contributor.author | Schultzberg, M. | en |
| dc.contributor.author | Iverfeldt, K. | en |
| dc.date.accessioned | 2015-11-24T19:10:41Z | |
| dc.date.available | 2015-11-24T19:10:41Z | |
| dc.identifier.issn | 0165-5728 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/20855 | |
| dc.rights | Default Licence | - |
| dc.subject | Animals | en |
| dc.subject | Cell Death/drug effects/immunology | en |
| dc.subject | Cell Survival/drug effects/immunology | en |
| dc.subject | Cerebellar Cortex/drug effects/immunology/*metabolism | en |
| dc.subject | Encephalitis/genetics/immunology/metabolism | en |
| dc.subject | Excitatory Amino Acid Antagonists/pharmacology | en |
| dc.subject | Glutamic Acid/*pharmacology | en |
| dc.subject | Mice | en |
| dc.subject | Mice, Knockout | en |
| dc.subject | Neurodegenerative Diseases/genetics/immunology/metabolism | en |
| dc.subject | Neurons/drug effects/immunology/*metabolism | en |
| dc.subject | Neurotoxins/*pharmacology | en |
| dc.subject | Receptors, Interleukin-1/*deficiency/genetics | en |
| dc.subject | Receptors, Interleukin-1 Type I | en |
| dc.subject | Receptors, N-Methyl-D-Aspartate/drug effects/*metabolism | en |
| dc.title | Increased sensitivity to N-methyl-D-aspartate receptor-induced excitotoxicity in cerebellar granule cells from interleukin-1 receptor type I-deficient mice | en |
| heal.abstract | The 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.access | campus | - |
| heal.fullTextAvailability | TRUE | - |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/12446013 | - |
| heal.journalName | J Neuroimmunol | en |
| heal.journalType | peer-reviewed | - |
| heal.language | en | - |
| heal.publicationDate | 2002 | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.type | journalArticle | - |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.type.en | Journal article | en |
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