2001
Multiple sclerosis: Altered glutamate homeostasis in lesions correlates with oligodendrocyte and axonal damage
Werner P, Pitt D, Raine C. Multiple sclerosis: Altered glutamate homeostasis in lesions correlates with oligodendrocyte and axonal damage. Annals Of Neurology 2001, 50: 169-180. PMID: 11506399, DOI: 10.1002/ana.1077.Peer-Reviewed Original ResearchConceptsMultiple sclerosisAxonal damageWhite matterGlutamate excitotoxicityGlutamate homeostasisMS lesionsGlutaminase expressionMS white matterInflammatory neurologic diseasesActive MS lesionsCNS cell typesOligodendroglial pathologyNoninflammatory conditionsDystrophic axonsNeurologic diseaseGLT-1Low-level expressionAnimal modelsGlutamate transportersHomeostasis contributesLesion correlatesGlutamate transportLesionsOligodendrocytesTherapeutic import
2000
Glutamate excitotoxicity in a model of multiple sclerosis
Pitt D, Werner P, Raine C. Glutamate excitotoxicity in a model of multiple sclerosis. Nature Medicine 2000, 6: 67-70. PMID: 10613826, DOI: 10.1038/71555.Peer-Reviewed Original ResearchConceptsGlutamate excitotoxicityMultiple sclerosisAMPA/kainate antagonist NBQXAMPA/kainate typeCentral nervous system inflammationAMPA/kainate antagonistAntigen-primed T cellsCentral nervous system2Nervous system inflammationExperimental autoimmune encephalomyelitisCentral nervous systemMyelin-producing cellsLack of effectDemyelinating modelKainate typeSystem inflammationAutoimmune encephalomyelitisInflammatory attacksKainate antagonistAntagonist NBQXAutoimmune demyelinationPathologic featuresClinical differencesReceptor damageOligodendrocyte survivalGlutamate excitotoxicity — a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis?
Werner P, Pitt D, Raine CS. Glutamate excitotoxicity — a mechanism for axonal damage and oligodendrocyte death in Multiple Sclerosis? Journal Of Neural Transmission. Supplementa 2000, 375-385. PMID: 11205156, DOI: 10.1007/978-3-7091-6301-6_27.Peer-Reviewed Original ResearchConceptsCentral nervous systemAMPA/kainate antagonistMultiple sclerosisGlutamate excitotoxicityImmune cellsKainate antagonistAxonal damageAntigen-primed T cellsMyelin-producing cellsLack of effectSite of entryCNS inflammationInflammatory attacksExperimental autoimmunePerivascular cuffsAutoimmune demyelinationInflammatory lesionsClinical differencesOligodendrocyte survivalEffective therapyGlutamate receptorsOligodendrocyte deathT cellsExcitotoxicityLesion size