2009
Dysmyelinated axons in shiverer mice are highly vulnerable to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity
Pitt D, Gonzales E, Cross AH, Goldberg MP. Dysmyelinated axons in shiverer mice are highly vulnerable to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity. Brain Research 2009, 1309: 146-154. PMID: 19896473, PMCID: PMC7343376, DOI: 10.1016/j.brainres.2009.10.066.Peer-Reviewed Original ResearchMeSH KeywordsAlpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsBiomarkersBrainDisease Models, AnimalExcitatory Amino Acid AgonistsFemaleHereditary Central Nervous System Demyelinating DiseasesLuminescent ProteinsMiceMice, Inbred C57BLMice, Neurologic MutantsMovement DisordersMyelin Basic ProteinNerve DegenerationNerve Fibers, MyelinatedNeurotoxinsN-MethylaspartateReceptors, AMPAConceptsNMDA receptorsShiverer miceAMPA/kainate receptorsLumbar dorsal columnWhite matter injuryWidespread axonal degenerationSpinal cord axonsActivation of receptorsReceptor-mediated toxicitySubset of axonsMyelin basic proteinAxonal vulnerabilityNeuroprotective therapiesGlutamate excitotoxicityNMDA injectionAxonal degenerationAxonal injuryDorsal columnsRotarod performanceAxon damageGlutamate toxicityCentral axonsGlial cellsS-AMPAAxonal toxicity
2004
Glutamate Excitotoxicity in Multiple Sclerosis
Pitt D, Raine C. Glutamate Excitotoxicity in Multiple Sclerosis. 2004, 285-303. DOI: 10.1007/978-1-4419-8959-8_16.Peer-Reviewed Original ResearchGlutamate excitotoxicityMultiple sclerosisWhite matter injuryCentral white matterProminent demyelinationMS pathogenesisOligodendrocyte damageInflammatory demyelinationOligodendrocyte lossExtracellular glutamateGlutamate homeostasisAnimal modelsExcitotoxicityWhite matterCell targetsClearance pathwaysCommon pathwayDisease mechanismsCell culture studiesDemyelinationSclerosisRecent dataOligodendrocytesCulture studiesPathogenesis
2003
Glutamate uptake by oligodendrocytes
Pitt D, Nagelmeier IE, Wilson HC, Raine CS. Glutamate uptake by oligodendrocytes. Neurology 2003, 61: 1113-1120. PMID: 14581674, DOI: 10.1212/01.wnl.0000090564.88719.37.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAstrocytesAutoradiographyBiological TransportCell SurvivalCells, CulturedDose-Response Relationship, DrugExcitatory Amino Acid Transporter 1Excitatory Amino Acid Transporter 2FemaleGene ExpressionGlutamic AcidHumansIn Situ HybridizationMaleMiddle AgedMultiple SclerosisNeurotoxinsOligodendrogliaRNA, MessengerSpinal CordTritiumTumor Necrosis Factor-alphaConceptsMS white matterEAAT-2EAAT-1White matterExtracellular glutamateGlutamate uptakePredominant cellsHuman oligodendrocytesGlutamate removalProinflammatory cytokine tumor necrosisHuman white matterNormal human white matterCommon pathologic eventGlutamate transporter expressionGlutamate receptor expressionCytokine tumor necrosisExcess extracellular glutamateInhibited glutamate uptakeHigh extracellular glutamateSubsequent overstimulationExcitotoxic damageGlutamate excitotoxicityGlutamate clearanceTumor necrosisReceptor expression
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 — 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 sizeGlutamate 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 survival