2018
Nav1.5 in astrocytes plays a sex‐specific role in clinical outcomes in a mouse model of multiple sclerosis
Pappalardo LW, Samad OA, Liu S, Zwinger PJ, Black JA, Waxman SG. Nav1.5 in astrocytes plays a sex‐specific role in clinical outcomes in a mouse model of multiple sclerosis. Glia 2018, 66: 2174-2187. PMID: 30194875, DOI: 10.1002/glia.23470.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesBrainCalcium-Binding ProteinsDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalFemaleGlial Fibrillary Acidic ProteinMaleMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsMonocytesMultiple SclerosisNAV1.5 Voltage-Gated Sodium ChannelSex CharacteristicsSpinal CordT-LymphocytesConceptsExperimental autoimmune encephalomyelitisMultiple sclerosisClinical outcomesSex-specific mannerInflammatory infiltrateEAE clinical scoreT cell infiltrationWT littermate controlsAutoimmune encephalomyelitisNeuroinflammatory disordersClinical courseClinical scoresAstroglial responseUnderlying molecular mechanismsSex-specific roleCell infiltrationFemale miceKO miceT cellsImmune responseMurine modelPossible dysregulationMouse modelLittermate controlsTherapeutic target
2007
Exacerbation of experimental autoimmune encephalomyelitis after withdrawal of phenytoin and carbamazepine
Black JA, Liu S, Carrithers M, Carrithers LM, Waxman SG. Exacerbation of experimental autoimmune encephalomyelitis after withdrawal of phenytoin and carbamazepine. Annals Of Neurology 2007, 62: 21-33. PMID: 17654737, DOI: 10.1002/ana.21172.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnticonvulsantsAntigens, CDAxonsCarbamazepineCell CountDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryGene Expression RegulationGlycoproteinsMiceMice, Inbred C57BLMyelin-Oligodendrocyte GlycoproteinNAV1.6 Voltage-Gated Sodium ChannelNerve Tissue ProteinsPeptide FragmentsPhenytoinPyramidal TractsSeverity of Illness IndexSodium ChannelsSubstance Withdrawal SyndromeConceptsExperimental autoimmune encephalomyelitisSodium channel blockersWithdrawal of phenytoinChannel blockersAutoimmune encephalomyelitisInflammatory infiltrateClinical studiesProtective effectMurine experimental autoimmune encephalomyelitisWithdrawal of carbamazepineCentral nervous system axonsCentral nervous systemAcute exacerbationAcute worseningClinical worseningEAE symptomsEAE miceNeuroinflammatory disordersClinical courseMyelin oligodendrocyteClinical statusControl miceMultiple sclerosisImmune cellsLong-term effects
2004
Sodium channels contribute to microglia/macrophage activation and function in EAE and MS
Craner MJ, Damarjian TG, Liu S, Hains BC, Lo AC, Black JA, Newcombe J, Cuzner ML, Waxman SG. Sodium channels contribute to microglia/macrophage activation and function in EAE and MS. Glia 2004, 49: 220-229. PMID: 15390090, DOI: 10.1002/glia.20112.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGliosisMacrophagesMaleMiceMice, Inbred C57BLMicrogliaMultiple SclerosisNAV1.6 Voltage-Gated Sodium ChannelNerve DegenerationNerve Tissue ProteinsNeuroprotective AgentsPhagocytosisPhenytoinRNA, MessengerSodium Channel BlockersSodium ChannelsTetrodotoxinUp-RegulationConceptsExperimental autoimmune encephalomyelitisMultiple sclerosisSodium channel blockersSodium channelsMicroglial activationChannel blockersPhagocytic capacityMicroglia/macrophage activationSpecific sodium channel blockerAcute MS lesionsDirect neuroprotective effectsPhagocytosis of microgliaActivation of microgliaAnti-inflammatory mechanismsSodium channel-blocking drugsInflammatory cell infiltrateLoss of axonsDisease multiple sclerosisSodium channel blockadeChannel-blocking drugsAxonal sodium channelsAutoimmune encephalomyelitisInflammatory mechanismsNeuroinflammatory disordersCell infiltrate