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
2016
Dendritic spine remodeling following early and late Rac1 inhibition after spinal cord injury: evidence for a pain biomarker
Zhao P, Hill M, Liu S, Chen L, Bangalore L, Waxman SG, Tan AM. Dendritic spine remodeling following early and late Rac1 inhibition after spinal cord injury: evidence for a pain biomarker. Journal Of Neurophysiology 2016, 115: 2893-2910. PMID: 26936986, PMCID: PMC4922610, DOI: 10.1152/jn.01057.2015.Peer-Reviewed Original ResearchConceptsSpinal cord injuryNeuropathic painDendritic spine dysgenesisDendritic spinesCord injurySpine dysgenesisDorsal horn neuronsSpine profilesDendritic spine remodelingEffective clinical translationSensory dysfunctionSignificant complicationsNociceptive systemPain biomarkersSpine remodelingClinical conditionsPreclinical studiesRac1 activityEffective treatmentPainDrug responsivenessStructural biomarkersDisease statesRac1 inhibitionBiomarkers
2014
Dynamics of sodium channel Nav1.5 expression in astrocytes in mouse models of multiple sclerosis
Pappalardo LW, Liu S, Black JA, Waxman SG. Dynamics of sodium channel Nav1.5 expression in astrocytes in mouse models of multiple sclerosis. Neuroreport 2014, 25: 1208-1215. PMID: 25144393, PMCID: PMC4159404, DOI: 10.1097/wnr.0000000000000249.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesEncephalomyelitis, Autoimmune, ExperimentalImmunohistochemistryLumbar VertebraeMice, BiozziMice, Inbred C57BLMotor CortexMultiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingNAV1.5 Voltage-Gated Sodium ChannelSeverity of Illness IndexSpinal CordUp-RegulationConceptsExperimental autoimmune encephalomyelitisCentral nervous systemMultiple sclerosisNervous systemChronic multiple sclerosis lesionsNav1.5 expressionPhases of relapsePeriods of remissionGlial scar formationResponse of astrocytesSeverity of diseasePotential therapeutic targetMultiple sclerosis lesionsVoltage-gated sodium channel Nav1.5Autoimmune encephalomyelitisNeuroinflammatory pathologiesIntracellular Ca levelsReactive astrogliosisGlial scarInflammatory pathologyMouse modelImmunohistochemical analysisScar formationTherapeutic targetAstrocytes
2013
Burn injury-induced mechanical allodynia is maintained by Rac1-regulated dendritic spine dysgenesis
Tan AM, Samad OA, Liu S, Bandaru S, Zhao P, Waxman SG. Burn injury-induced mechanical allodynia is maintained by Rac1-regulated dendritic spine dysgenesis. Experimental Neurology 2013, 248: 509-519. PMID: 23933578, DOI: 10.1016/j.expneurol.2013.07.017.Peer-Reviewed Original ResearchConceptsDendritic spine dysgenesisWDR neuronsNeuropathic painBurn injurySpine dysgenesisMechanical allodyniaInjury-induced chronic painInjury-induced mechanical allodyniaSpinal cord dorsal hornBurn-injured animalsHindpaw receptive fieldsInjury-induced painNeuropathic pain phenotypesSecond-degree burn injurySecond-degree burn modelDendritic spine morphologyDendritic spine shapeDorsal hornIntractable painMechanical painPain managementChronic painPain phenotypesElectrophysiological signsPreclinical models
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