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
2010
Slowly Progressive Axonal Degeneration in a Rat Model of Chronic, Nonimmune-Mediated Demyelination
Wilkins A, Kondo Y, Song J, Liu S, Compston A, Black J, Waxman S, Duncan I. Slowly Progressive Axonal Degeneration in a Rat Model of Chronic, Nonimmune-Mediated Demyelination. Journal Of Neuropathology & Experimental Neurology 2010, 69: 1256-1269. PMID: 21107138, DOI: 10.1097/nen.0b013e3181ffc317.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsChronic DiseaseDemyelinating DiseasesDisease Models, AnimalDisease ProgressionMicrotubulesNerve DegenerationRatsRats, TransgenicTime FactorsConceptsCentral nervous systemAxonal lossAxonal degenerationAxonal pathologyTrophic supportEarly axonal lossProgressive axonal lossProgressive axonal degenerationWhite matter tractsTaiep mutant ratNerve countsWild-type controlsChronic demyelinationNeurologic disabilityMyelin lossSignificant inflammationRat modelOligodendrocyte dysfunctionImmunohistochemical analysisTaiep ratsNervous systemCNS regionsAxonal transportMutant ratsOligodendrocyte lineage
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
Changes in the expression of tetrodotoxin‐sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain
Black JA, Liu S, Tanaka M, Cummins TR, Waxman SG. Changes in the expression of tetrodotoxin‐sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain. Pain 2004, 108: 237-247. PMID: 15030943, DOI: 10.1016/j.pain.2003.12.035.Peer-Reviewed Original ResearchMeSH KeywordsAnesthetics, LocalAnimalsBlotting, WesternCarrageenanCells, CulturedDisease Models, AnimalFunctional LateralityGanglia, SpinalGene Expression RegulationImmunohistochemistryIn Situ HybridizationInflammationMaleMembrane PotentialsNeuronsPainPatch-Clamp TechniquesRatsRats, Sprague-DawleyRNA, MessengerSodium ChannelsTetrodotoxinConceptsTTX-R currentsDorsal root gangliaDRG neuronsInflammatory painSodium channelsCarrageenan injectionProstaglandin E2TTX-R sodium channelsTetrodotoxin-sensitive sodium channelsDorsal root ganglion neuronsMultiple voltage-gated sodium channelsWhole-cell patch-clamp methodTTX-S sodium channelsTTX-R channelsTTX-S currentsSmall DRG neuronsInjection of carrageenanTTX-S channelsChronic inflammation resultsTetrodotoxin-resistant channelsVoltage-gated sodium channelsPatch-clamp methodUpregulation of mRNAAffected pawAcute administrationSodium 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