2012
Axonal Protection with Sodium Channel Blocking Agents in Models of Multiple Sclerosis
Black J, Smith K, Waxman S. Axonal Protection with Sodium Channel Blocking Agents in Models of Multiple Sclerosis. 2012, 179-201. DOI: 10.1007/978-1-4614-2218-1_8.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisMultiple sclerosisSodium channelsAspects of MSAcute MS plaquesChronic inactive plaquesSignificant axonal damageImmune cell infiltrationSodium channel blockadeChannel Blocking AgentsSpinal cord axonsWhite matter axonsVoltage-gated sodium channelsAction potential conductionInactive plaquesClinical disabilityAutoimmune encephalomyelitisAxonal protectionNeuroinflammatory disordersNeurological deficitsNeuroprotective therapiesAxonal damageIschemia injuryAxonal degenerationAxonal injury
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 ResearchConceptsCentral 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
2006
Axonal conduction and injury in multiple sclerosis: the role of sodium channels
Waxman SG. Axonal conduction and injury in multiple sclerosis: the role of sodium channels. Nature Reviews Neuroscience 2006, 7: 932-941. PMID: 17115075, DOI: 10.1038/nrn2023.Peer-Reviewed Original ResearchConceptsAxonal degenerationSodium channelsChannel isoformsDistinct pathophysiological rolesKey PointsMultiple sclerosisMultiple neurological deficitsRelapsing-remitting courseRestoration of conductionDegeneration of axonsCerebellar Purkinje neuronsVoltage-gated sodium channelsContext of demyelinationNeurological deficitsProgressive courseMultiple sclerosisAxonal conductionDisease progressionNav1.8 channelsConduction failurePathophysiological rolePurkinje neuronsCNS axonsFiring patternsLoss of coordinationAberrant expression
2005
22 Neuronal Blocking Factors in Demyelinating Diseases
Cummins T, Waxman S. 22 Neuronal Blocking Factors in Demyelinating Diseases. 2005, 317-326. DOI: 10.1016/b978-012738761-1/50023-7.Peer-Reviewed Original ResearchVoltage-gated sodium channelsGuillain-Barré syndromeMultiple sclerosisSodium channelsChronic inflammatory demyelinating polyneuropathyInflammatory demyelinating polyneuropathyInflammatory demyelinating diseaseBlocking factorsDemyelinating polyneuropathyDemyelinating diseaseClinical deficitsAxonal degenerationInflammatory diseasesConduction blockSodium currentNitric oxideExperimental modelDiseaseImpulse transmissionSclerosisBiological toxinsDemyelinationFactorsPolyneuropathyCytokines19 Molecular Mechanisms of Calcium Influx in Axonal Degeneration
Stys P, Waxman S. 19 Molecular Mechanisms of Calcium Influx in Axonal Degeneration. 2005, 275-292. DOI: 10.1016/b978-012738761-1/50020-1.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisAxonal degenerationMultiple sclerosisAxonal injuryCalcium influxInflammatory central nervous system disordersCentral nervous system disordersAcute axonal injuryPotential neuroprotective strategiesWhite matter injuryCellular calcium overloadNervous system disordersAutoimmune encephalomyelitisAxonal damageNeuroprotective strategiesGlutamate releasePathophysiological mechanismsCa overloadCalcium overloadSystem disordersInadequate deliveryMyelinated axonsAberrant operationNitric oxideCa channels7 Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and its Models
Waxman S. 7 Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and its Models. 2005, 101-118. DOI: 10.1016/b978-012738761-1/50008-0.Peer-Reviewed Original ResearchMultiple sclerosisSodium channel subtypesVoltage-gated sodium channelsSodium channelsChannel subtypesDistinct voltage-gated sodium channelsPathophysiology of MSAxonal degenerationTherapeutic strategiesSclerosisFiring patternsExperimental modelMaladaptive roleNeuronal signalingSubtypesMolecular analysisAltered distributionNeuronsRecent studiesMajor contributorPathophysiologyAxonsDegenerationDiseaseImportant role
2000
Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis
Black J, Dib-Hajj S, Baker D, Newcombe J, Cuzner M, Waxman S. Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 11598-11602. PMID: 11027357, PMCID: PMC17246, DOI: 10.1073/pnas.97.21.11598.Peer-Reviewed Original ResearchConceptsExperimental allergic encephalomyelitisMultiple sclerosisAllergic encephalomyelitisClinical abnormalitiesChannel expressionPurkinje cellsTrigeminal ganglion neuronsBrains of micePeripheral nervous systemSodium channel expressionIon channel expressionCerebellar Purkinje cellsAbnormal repertoiresAxonal degenerationControl miceGanglion neuronsControl subjectsMouse modelNormal brainAnimal modelsNervous systemNeurological diseasesSodium channelsProtein expressionAbnormal patterns