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
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