2014
Tapered withdrawal of phenytoin removes protective effect in EAE without inflammatory rebound and mortality
Liu S, Zwinger P, Black JA, Waxman SG. Tapered withdrawal of phenytoin removes protective effect in EAE without inflammatory rebound and mortality. Journal Of The Neurological Sciences 2014, 341: 8-12. PMID: 24690348, DOI: 10.1016/j.jns.2014.03.029.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisSodium channel blockersImmune cell infiltratesMultiple sclerosisChannel blockersNeurological deficitsPhenytoin treatmentCell infiltrateTapered withdrawalTreatment of MSModel of MSSudden withdrawalMassive inflammatory infiltrateNon-treated levelsPotential therapeutic agentInflammatory reboundSevere exacerbationsAutoimmune encephalomyelitisNeuroprotective therapiesInflammatory infiltrateClinical scoresAbrupt withdrawalProtective effectHigh mortalityInfiltrates
2008
Sodium channel activity modulates multiple functions in microglia
Black JA, Liu S, Waxman SG. Sodium channel activity modulates multiple functions in microglia. Glia 2008, 57: 1072-1081. PMID: 19115387, DOI: 10.1002/glia.20830.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsAnimals, NewbornBrainCell MovementCell ProliferationCells, CulturedCoculture TechniquesCytokinesGliosisInflammation MediatorsMicrogliaNAV1.1 Voltage-Gated Sodium ChannelNAV1.5 Voltage-Gated Sodium ChannelNAV1.6 Voltage-Gated Sodium ChannelNerve Tissue ProteinsPhagocytosisPhenytoinRatsRats, Sprague-DawleySodium Channel BlockersSodium ChannelsTetrodotoxinConceptsIL-1 betaIL-1 alphaSodium channelsTNF-alphaPhagocytic activitySodium channel blockadeSodium channel Nav1.1Central nervous systemVoltage-gated sodium channelsSodium channel activitySodium channel isoformsActivated microgliaIL-10IL-6MCP-1Microglial migrationChannel Nav1.1Cultured microgliaIL-2IL-4MicroM TTXChannel blockadeMed miceMicrogliaTissue insult
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
2006
Long-term protection of central axons with phenytoin in monophasic and chronic-relapsing EAE
Black JA, Liu S, Hains BC, Saab CY, Waxman SG. Long-term protection of central axons with phenytoin in monophasic and chronic-relapsing EAE. Brain 2006, 129: 3196-3208. PMID: 16931536, DOI: 10.1093/brain/awl216.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAdministration, OralAnimalsAxonsCell CountCervical VertebraeChronic DiseaseEncephalomyelitis, Autoimmune, ExperimentalImmunohistochemistryInjections, SubcutaneousMiceMice, Inbred C57BLMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNeural ConductionPhenytoinRecurrenceSodium Channel BlockersSpinal CordTreatment OutcomeConceptsExperimental autoimmune encephalomyelitisC57/BL6 miceChronic-relapsing experimental autoimmune encephalomyelitisBL6 miceLong-term protectionAxonal degenerationClinical statusDays post-EAE inductionMurine experimental autoimmune encephalomyelitisLong-term protective effectPhenytoin-treated miceInflammatory cell infiltrationDorsal column axonsCompound action potentialSodium channel blockersAutoimmune encephalomyelitisAxonal lossPhenytoin treatmentUntreated miceNeuroinflammatory diseasesDorsal columnsMultiple sclerosisCNS injuryCell infiltrationCorticospinal tract
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