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dc.contributor.authorAkyildiz, A
dc.contributor.authorBelce, Ahmet
dc.contributor.authorBarut, S
dc.contributor.authorTasyurekli, Mustafa
dc.contributor.authorUzun, Hafize
dc.contributor.authorColak, A
dc.contributor.authorSoy, O
dc.contributor.authorAslan, O
dc.date.accessioned2021-03-03T14:39:39Z
dc.date.available2021-03-03T14:39:39Z
dc.date.issued2003
dc.identifier.citationColak A., Soy O., Uzun H., Aslan O., Barut S., Belce A., Akyildiz A., Tasyurekli M., "Neuroprotective effects of GYKI 52466 on experimental spinal cord injury in rats", JOURNAL OF NEUROSURGERY, cilt.98, sa.3, ss.275-281, 2003
dc.identifier.issn0022-3085
dc.identifier.otherav_3abc5d14-25e7-431d-afb1-64356502c4f0
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/43469
dc.identifier.urihttps://doi.org/10.3171/spi.2003.98.3.0275
dc.description.abstractObject. The toxic effects of glutamate in the central nervous system are well known. This neurotoxicity occurs through metabotropic and ionotropic receptors, the latter group composed of N-methyl-D-aspartate, alpha-amino-3hydroxy-5-methylisoxazole-4-proprionic acid (AMPA), and kainate receptors. The authors investigated the neuroprotective effects of GYKI 52466, a 2,3-benzodiazepine that is a selective and potent AMPA receptor antagonist, in a rat spinal cord trauma model.
dc.language.isoeng
dc.subjectCerrahi Tıp Bilimleri
dc.subjectTıp
dc.subjectNöroloji
dc.subjectSağlık Bilimleri
dc.subjectDahili Tıp Bilimleri
dc.subjectCERRAHİ
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectKLİNİK NEUROLOJİ
dc.titleNeuroprotective effects of GYKI 52466 on experimental spinal cord injury in rats
dc.typeMakale
dc.relation.journalJOURNAL OF NEUROSURGERY
dc.contributor.department, ,
dc.identifier.volume98
dc.identifier.issue3
dc.identifier.startpage275
dc.identifier.endpage281
dc.contributor.firstauthorID18642


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