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
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
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