2012
Hodgkin and Huxley and the basis for electrical signalling: a remarkable legacy still going strong
Vandenberg J, Waxman S. Hodgkin and Huxley and the basis for electrical signalling: a remarkable legacy still going strong. The Journal Of Physiology 2012, 590: 2569-2570. PMID: 22787169, PMCID: PMC3424715, DOI: 10.1113/jphysiol.2012.233411.Peer-Reviewed Original Research
2009
The ataxia3 Mutation in the N-Terminal Cytoplasmic Domain of Sodium Channel Nav1.6 Disrupts Intracellular Trafficking
Sharkey LM, Cheng X, Drews V, Buchner DA, Jones JM, Justice MJ, Waxman SG, Dib-Hajj SD, Meisler MH. The ataxia3 Mutation in the N-Terminal Cytoplasmic Domain of Sodium Channel Nav1.6 Disrupts Intracellular Trafficking. Journal Of Neuroscience 2009, 29: 2733-2741. PMID: 19261867, PMCID: PMC2679640, DOI: 10.1523/jneurosci.6026-08.2009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell LineChromosome MappingCytoplasmData Interpretation, StatisticalDNA, ComplementaryElectrophysiologyEthylnitrosoureaImmunohistochemistryMachado-Joseph DiseaseMiceMice, Inbred C57BLMutagensMutationMutation, MissenseNAV1.6 Voltage-Gated Sodium ChannelNerve Tissue ProteinsPatch-Clamp TechniquesSciatic NerveSodium ChannelsSubcellular FractionsTransfectionConceptsMutant channelsCytoplasmic N-terminal regionN-terminal cytoplasmic domainCytoplasmic N-terminal domainMouse chromosome 15N-terminal domainN-terminal regionAmino acid substitution p.Primary cerebellar granule cellsVoltage-dependent inward sodium currentMutant proteinsCytoplasmic domainJuvenile lethalityCis-GolgiTrafficking defectsPlasma membraneSodium channelsIntracellular traffickingProtein abundanceWild typeN-terminusGolgi complexMutant transcriptsChromosome 15Whole-cell patch-clamp studies
2002
Nitric Oxide Blocks Fast, Slow, and Persistent Na+ Channels in C-Type DRG Neurons by S-Nitrosylation
Renganathan M, Cummins T, Waxman S. Nitric Oxide Blocks Fast, Slow, and Persistent Na+ Channels in C-Type DRG Neurons by S-Nitrosylation. Journal Of Neurophysiology 2002, 87: 761-775. PMID: 11826045, DOI: 10.1152/jn.00369.2001.Peer-Reviewed Original ResearchConceptsSteady-state voltage-dependent inactivationDorsal root ganglion neuronsNitric oxide blockIncubation of neuronsNO scavenger hemoglobinSlow sodium channel inactivationNitric oxide donorFast TTXMembrane-permeable analogSlow TTXVoltage-dependent inactivationDRG neuronsGanglion neuronsSodium channel inactivationCurrent inhibitionOxide donorScavenger hemoglobinPersistent TTXPAPA-NONOateS-nitrosoTTXNeuronsChannel inactivationSlow inactivationCGMP-dependent protein kinase
2001
Contribution of Nav1.8 Sodium Channels to Action Potential Electrogenesis in DRG Neurons
Renganathan M, Cummins T, Waxman S. Contribution of Nav1.8 Sodium Channels to Action Potential Electrogenesis in DRG Neurons. Journal Of Neurophysiology 2001, 86: 629-640. PMID: 11495938, DOI: 10.1152/jn.2001.86.2.629.Peer-Reviewed Original ResearchConceptsAction potential electrogenesisDRG neuronsSodium channelsAction potentialsTTX-R sodium channelsSodium-dependent action potentialsDorsal root ganglion neuronsMultiple sodium channelsSmall DRG neuronsCurrent-clamp recordingsNav1.8 sodium channelsSignificant differencesSteady-state inactivationAction potential overshootMaximum rise slopeMV/msAction potential productionFast TTXGanglion neuronsModest depolarizationNeuronsInput resistanceMembrane depolarizationInward membraneElectrogenesis
1999
Sodium channels: from mechanisms to medicines?
Waxman S, Wood J. Sodium channels: from mechanisms to medicines? Brain Research Bulletin 1999, 50: 309-310. PMID: 10643411, DOI: 10.1016/s0361-9230(99)00158-6.Peer-Reviewed Original ResearchSodium channels, excitability of primary sensory neurons, and the molecular basis of pain
Waxman S, Cummins T, Dib‐Hajj S, Fjell J, Black J. Sodium channels, excitability of primary sensory neurons, and the molecular basis of pain. Muscle & Nerve 1999, 22: 1177-1187. PMID: 10454712, DOI: 10.1002/(sici)1097-4598(199909)22:9<1177::aid-mus3>3.0.co;2-p.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsPrimary sensory neuronsDRG neuronsSodium channel expressionSodium channel gene expressionSensory neuronsChannel gene expressionSodium channelsChannel expressionSodium currentTTX-sensitive sodium currentAbnormal burst activityNormal DRG neuronsSNS/PN3Resistant sodium currentsDistinct sodium channelsSodium channel geneChannel genesInflammatory painNerve injuryAxonal transectionElectrophysiological abnormalitiesSelective blockadePharmacological approachesBurst activityPainCharacterization of a new sodium channel mutation at arginine 1448 associated with moderate paramyotonia congenita in humans
Bendahhou S, Cummins T, Kwiecinski H, Waxman S, Ptácek L. Characterization of a new sodium channel mutation at arginine 1448 associated with moderate paramyotonia congenita in humans. The Journal Of Physiology 1999, 518: 337-344. PMID: 10381583, PMCID: PMC2269438, DOI: 10.1111/j.1469-7793.1999.0337p.x.Peer-Reviewed Original ResearchConceptsChannel functionMutant channelsHuman embryonic kidney 293 cellsEmbryonic kidney 293 cellsSodium channel alpha subunitAmino acid changesSingle nucleotide substitutionKidney 293 cellsChannel alpha subunitSkeletal muscle voltage-gated sodium channelPosition 1448Sodium channel mutationsParamyotonia congenitaVoltage-gated sodium channelsSodium channel functionNucleotide substitutionsAlpha subunitSingle-strand conformation polymorphism analysisSegment S4Skeletal muscle disordersDomain IVAcid changesNew genetic mutationsDNA sequencingFast inactivation
1998
Transplanted Olfactory Ensheathing Cells Remyelinate and Enhance Axonal Conduction in the Demyelinated Dorsal Columns of the Rat Spinal Cord
Imaizumi T, Lankford K, Waxman S, Greer C, Kocsis J. Transplanted Olfactory Ensheathing Cells Remyelinate and Enhance Axonal Conduction in the Demyelinated Dorsal Columns of the Rat Spinal Cord. Journal Of Neuroscience 1998, 18: 6176-6185. PMID: 9698311, PMCID: PMC2605360, DOI: 10.1523/jneurosci.18-16-06176.1998.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsElectrophysiologyFemaleMyelin SheathNeural ConductionNeuronsOlfactory NerveRatsRats, WistarSpinal CordConceptsDorsal column axonsRat spinal cordSpinal cordRemyelinated axonsDorsal columnsAdult rat spinal cordExtent of remyelinationTransplantation of OECsSpinal cord lesionsCell injection siteQuantitative histological analysisFunctional remyelinationCord lesionsAxonal conductionNeonatal ratsFocal injectionsConduction blockSchwann cellsConduction velocityInjection siteElectrophysiological propertiesAction potentialsAxonsHistological analysisTransplantation
1997
TTX-Sensitive and -Resistant Na+ Currents, and mRNA for the TTX-Resistant rH1 Channel, Are Expressed in B104 Neuroblastoma Cells
Gu X, Dib-Hajj S, Rizzo M, Waxman S. TTX-Sensitive and -Resistant Na+ Currents, and mRNA for the TTX-Resistant rH1 Channel, Are Expressed in B104 Neuroblastoma Cells. Journal Of Neurophysiology 1997, 77: 236-246. PMID: 9120565, DOI: 10.1152/jn.1997.77.1.236.Peer-Reviewed Original ResearchConceptsB104 neuroblastoma cellsTTX-resistant channelsB104 cellsNeuroblastoma cellsWhole-cell patch-clamp methodAbsence of TTXTTX-resistant currentTTX-sensitive currentsPresence of TTXPA/pFTranscription-polymerase chain reactionLong QT syndromeCell linesSteady-state inactivationNeuroblastoma cell linesAlpha-subunit mRNAPatch-clamp methodTTX-sensitiveHalf-maximal inhibitionInactivation time constantsChannel mRNATTXMembrane excitabilitySubunit mRNAsRT-PCR
1996
Manipulation of the delayed rectifier Kv1.5 potassium channel in glial cells by antisense oligodeoxynucleotides
Roy M, Saal D, Perney T, Sontheimer H, Waxman S, Kaczmarek L. Manipulation of the delayed rectifier Kv1.5 potassium channel in glial cells by antisense oligodeoxynucleotides. Glia 1996, 18: 177-184. PMID: 8915650, DOI: 10.1002/(sici)1098-1136(199611)18:3<177::aid-glia2>3.0.co;2-x.Peer-Reviewed Original ResearchConceptsGlial cellsKv1.5 channel proteinSpinal cordKv1.5 proteinCultured spinal cordTEA-insensitive currentSpinal cord astrocytesRectifier current densityPotassium channel typesAntisense oligodeoxynucleotide treatmentKv1.5 potassium channelAdult ratsCerebellar slicesChannel proteinsAstrocytesOligodeoxynucleotide treatmentPotassium channelsRectifier currentEndfoot processesSuch treatmentCurrent activationAntisense oligodeoxynucleotidesCordCellsTreatmentVoltage-gated Na+ channels in glia: properties and possible functions
Sontheimer H, Black J, Waxman S. Voltage-gated Na+ channels in glia: properties and possible functions. Trends In Neurosciences 1996, 19: 325-331. PMID: 8843601, DOI: 10.1016/0166-2236(96)10039-4.Peer-Reviewed Original Research
1994
Activity‐dependent modulation of excitability: Implications for axonal physiology and pathophysiology
Stys P, Waxman S. Activity‐dependent modulation of excitability: Implications for axonal physiology and pathophysiology. Muscle & Nerve 1994, 17: 969-974. PMID: 7520532, DOI: 10.1002/mus.880170902.Peer-Reviewed Original ResearchAstrocyte Na+ channels are required for maintenance of Na+/K(+)-ATPase activity
Sontheimer H, Fernandez-Marques E, Ullrich N, Pappas C, Waxman S. Astrocyte Na+ channels are required for maintenance of Na+/K(+)-ATPase activity. Journal Of Neuroscience 1994, 14: 2464-2475. PMID: 8182422, PMCID: PMC6577452, DOI: 10.1523/jneurosci.14-05-02464.1994.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornAstrocytesAstrocytomaCell LineCells, CulturedElectrophysiologyGanglia, SpinalGliomaMembrane PotentialsModels, BiologicalOuabainRatsRats, Sprague-DawleyRubidiumSodiumSodium ChannelsSodium-Potassium-Exchanging ATPaseStrophanthidinTetrodotoxinTime FactorsTumor Cells, CulturedConceptsEffects of TTXGlial cellsAction potential electrogenesisRat spinal cordPatch-clamp recordingsAstrocyte membrane potentialDose-dependent mannerVoltage-activated channelsAcute blockadeSpinal cordVoltage-activated ion channelsSpecific blockerATPase activityAstrocytesTTXAstrocyte deathAction potentialsUnidirectional influxBlockadeExcitable cellsIon channelsOuabainExtracellular spaceMembrane potentialIon levels
1993
Molecular dissection of the myelinated axon
Waxman S, Ritchie J. Molecular dissection of the myelinated axon. Annals Of Neurology 1993, 33: 121-136. PMID: 7679565, DOI: 10.1002/ana.410330202.Peer-Reviewed Original ResearchConceptsMyelinated axonsInternodal axon membraneDemyelinated axonsCentral nervous system white matterNervous system white matterRestoration of conductionImportant therapeutic approachSchwann cell processesWhite matter axonsInflux of Ca2Important pathophysiological implicationsGlial cell processesAction potential conductionAxonal excitabilityGlial cellsAnoxic injuryMyelinated fibersTherapeutic approachesAstrocyte processesCell processesPathophysiological implicationsRepetitive firingWhite matterNeurological disordersAction potentials
1992
Chapter 8: The expression of sodium channels in astrocytes in situ and in vitro
Black J, Sontheimer H, Minturn J, Ransom B, Waxman S. Chapter 8: The expression of sodium channels in astrocytes in situ and in vitro. Progress In Brain Research 1992, 94: 89-107. PMID: 1337617, DOI: 10.1016/s0079-6123(08)61742-2.Peer-Reviewed Original ResearchConceptsOptic nerve astrocytesSodium channel expressionChannel expressionSodium channelsOptic nerveSodium current propertiesChannel expression patternsIon channel expressionSimilar electrophysiological propertiesCultured astrocytesAstrocytesElectrophysiological propertiesSodium currentHeterogeneous groupDifferent patternsNerveDifferent subpopulationsExpressionExpression patternsCell-cell interactionsHippocampusA2B5Neurons
1985
Rat optic nerve: Disruption of gliogenesis with 5-azacytidine during early postnatal development
Ransom B, Yamate C, Black J, Waxman S. Rat optic nerve: Disruption of gliogenesis with 5-azacytidine during early postnatal development. Brain Research 1985, 337: 41-49. PMID: 2408709, DOI: 10.1016/0006-8993(85)91607-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornAzacitidineElectrophysiologyEvoked Potentials, VisualMyelin SheathNeurogliaOptic NerveRatsRats, Inbred StrainsConceptsOptic nerveGlial cellsOptic nerve axonsRat optic nerveCompound action potentialEarly postnatal developmentDays of ageOlder nervesNeonatal treatmentBrain extracellular spaceNeuroglial interactionsElectrophysiological studiesNervePostnatal developmentAction potentialsNerve axonsExcitability propertiesMarked reductionMyelin formationGliogenesisMitotic inhibitorsIonic homeostasisExtracellular spaceAgeAnimalsLigature‐induced injury in peripheral nerve: Electrophysiological observations on changes in action potential characteristics following blockade of potassium conductance
Waxman S, Kocsis J, Eng D. Ligature‐induced injury in peripheral nerve: Electrophysiological observations on changes in action potential characteristics following blockade of potassium conductance. Muscle & Nerve 1985, 8: 85-92. PMID: 2414652, DOI: 10.1002/mus.880080202.Peer-Reviewed Original ResearchConceptsAction potentialsRepetitive firingSingle stimulusPotassium channelsCompound action potentialRat sciatic nerveAction potential propertiesWhole-nerve responseAction potential characteristicsIntra-axonal recordingsAction potential waveformNerve segmentsSciatic nerveNerve responsesPeripheral nervesInjury siteMyelinated fibersLater spikesElectrophysiological observationsNerveRefractory periodFiring patternsPotassium conductancePotential waveformInitial spike
1984
Cell death of asynaptic neurons in regenerating spinal cord
Anderson M, Waxman S, Tadlock C. Cell death of asynaptic neurons in regenerating spinal cord. Developmental Biology 1984, 103: 443-455. PMID: 6724138, DOI: 10.1016/0012-1606(84)90332-4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell CountCell SurvivalElectric OrganElectrophysiologyFishesMicroscopy, ElectronMotor NeuronsNerve RegenerationSpinal CordSynapsesConceptsSpinal cordElectromotor neuronsRegenerated cordNormal numbersNumber of perikaryaCell deathCaudal endRostro-caudal axisSpinal neuronsCordCell bodiesNeuronsSynaptic competitionAxonsNumerous cellsDeathPerikaryaAmputationMore yearsEvidence of migrationSternarchus albifronsExcess numberElectric organEpendymaTransverse sections
1981
Electrophysiology of demyelinating diseases: future directions and questions.
Waxman S, Ritchie J. Electrophysiology of demyelinating diseases: future directions and questions. Advances In Neurology 1981, 31: 511-13. PMID: 6275675.Peer-Reviewed Original ResearchCellular aspects of conduction in myelinated nerve fibers in relation to clinical deficit.
Waxman S. Cellular aspects of conduction in myelinated nerve fibers in relation to clinical deficit. Progress In Clinical And Biological Research 1981, 52: 1-15. PMID: 7232439.Peer-Reviewed Original Research