2018
Nonmuscle myosin II isoforms interact with sodium channel alpha subunits
Dash B, Han C, Waxman S, Dib-Hajj S. Nonmuscle myosin II isoforms interact with sodium channel alpha subunits. Molecular Pain 2018, 14: 1744806918788638. PMID: 29956586, PMCID: PMC6052497, DOI: 10.1177/1744806918788638.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsAnkyrinsBrainCell Line, TransformedElectric StimulationGanglia, SpinalGene Expression RegulationGreen Fluorescent ProteinsHumansImmunoprecipitationMiceMice, Inbred C57BLMice, TransgenicMolecular Motor ProteinsMyosin Heavy ChainsNAV1.6 Voltage-Gated Sodium ChannelNonmuscle Myosin Type IIBPatch-Clamp TechniquesRatsTransfectionConceptsSodium channel alpha subunitND7/23 cellsChannel alpha subunitDorsal root ganglion tissueAlpha subunitMyosin II motor proteinsNonmuscle myosin II isoformsRodent nervous tissueRodent brain tissueSteady-state fast inactivationVoltage-sensitive channelsFast inactivationVoltage-dependent activationSodium channel alphaGanglion tissueIsoform-dependent mannerMyosin II isoformsNervous tissueRecombinant myosinBrain tissueCommon structural motifRamp currentsMotor proteinsCellular excitabilitySodium channels
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
2001
Glycosylation Alters Steady-State Inactivation of Sodium Channel Nav1.9/NaN in Dorsal Root Ganglion Neurons and Is Developmentally Regulated
Tyrrell L, Renganathan M, Dib-Hajj S, Waxman S. Glycosylation Alters Steady-State Inactivation of Sodium Channel Nav1.9/NaN in Dorsal Root Ganglion Neurons and Is Developmentally Regulated. Journal Of Neuroscience 2001, 21: 9629-9637. PMID: 11739573, PMCID: PMC6763018, DOI: 10.1523/jneurosci.21-24-09629.2001.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsAnimals, NewbornAntibody SpecificityAxotomyCell MembraneCells, CulturedFemaleGanglia, SpinalGlycosylationImmunoblottingMembrane PotentialsN-Acetylneuraminic AcidNAV1.9 Voltage-Gated Sodium ChannelNeuraminidaseNeuronsNeuropeptidesPatch-Clamp TechniquesRatsRats, Sprague-DawleySciatic NerveSodiumSodium ChannelsSubcellular FractionsTetrodotoxinTrigeminal GanglionConceptsImmunoreactive proteinMembrane fractionAdult DRG neuronsTranscription-PCR analysisHigh molecular weight immunoreactive proteinTheoretical molecular weightWhole-cell patch-clamp analysisLong transcriptsGlycosylation statePatch-clamp analysisAdult tissuesLarge proteinsLimited glycosylationEnzymatic deglycosylationExtensive glycosylationState of glycosylationProteinAdult dorsal root gangliaGlycosylationNative neuronsDevelopmental changesInactivationMembrane preparationsDRG neuronsDorsal root ganglia
2000
Development of Glutamatergic Synaptic Activity in Cultured Spinal Neurons
Robert A, Howe J, Waxman S. Development of Glutamatergic Synaptic Activity in Cultured Spinal Neurons. Journal Of Neurophysiology 2000, 83: 659-670. PMID: 10669482, DOI: 10.1152/jn.2000.83.2.659.Peer-Reviewed Original ResearchMeSH Keywords2-Amino-5-phosphonovalerate6-Cyano-7-nitroquinoxaline-2,3-dioneAnimalsCells, CulturedExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsFetusGlutamic AcidMagnesiumMembrane PotentialsNeuronsPatch-Clamp TechniquesQuinoxalinesRatsRats, Sprague-DawleyReceptors, AMPAReceptors, N-Methyl-D-AspartateSpinal CordSynapsesTetrodotoxinConceptsSpontaneous synaptic activityCultured spinal neuronsSynaptic activitySpinal neuronsGlutamatergic synapsesSynaptic currentsGlutamatergic synaptic activityIsoxazolepropionic acid (AMPA) receptorsSpontaneous synaptic currentsOlder neuronsSynaptic NMDARsExogenous glutamateNMDARAcid receptorsSynaptic regionNeuronsReceptor openingSignificant increaseTime courseSynapsesSequence of eventsActivityWeeksCourseReceptors
1999
Characterization 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 inactivationSodium channel expression in NGF‐overexpressing transgenic mice
Fjell J, Cummins T, Davis B, Albers K, Fried K, Waxman S, Black J. Sodium channel expression in NGF‐overexpressing transgenic mice. Journal Of Neuroscience Research 1999, 57: 39-47. PMID: 10397634, DOI: 10.1002/(sici)1097-4547(19990701)57:1<39::aid-jnr5>3.0.co;2-m.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedGanglia, SpinalMiceMice, Inbred C57BLMice, TransgenicNerve Growth FactorsNeuronsPatch-Clamp TechniquesRNA, MessengerSodium ChannelsConceptsNerve growth factorSodium channel expressionWild-type miceDRG neuronsTransgenic miceChannel expressionLevels of NGFDorsal root ganglion neuronsSNS/PN3Whole-cell patch-clamp studiesSmall DRG neuronsPeripheral nervous systemSodium channel mRNAFunctional sodium channelsPeak sodium current densityRegulation of expressionSodium current densityPatch-clamp studiesMechanical hyperalgesiaEmbryonic day 11Ganglion neuronsMouse DRGWild-type DRGsNervous systemLong-term overexpressionActivation and Inactivation of the Voltage-Gated Sodium Channel: Role of Segment S5 Revealed by a Novel Hyperkalaemic Periodic Paralysis Mutation
Bendahhou S, Cummins T, Tawil R, Waxman S, Ptácek L. Activation and Inactivation of the Voltage-Gated Sodium Channel: Role of Segment S5 Revealed by a Novel Hyperkalaemic Periodic Paralysis Mutation. Journal Of Neuroscience 1999, 19: 4762-4771. PMID: 10366610, PMCID: PMC6782655, DOI: 10.1523/jneurosci.19-12-04762.1999.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedDNA Mutational AnalysisDNA PrimersGene ExpressionHumansHyperkalemiaIon Channel GatingKidneyKineticsMaleMiddle AgedMolecular Sequence DataNAV1.4 Voltage-Gated Sodium ChannelParalyses, Familial PeriodicPatch-Clamp TechniquesPoint MutationProtein Structure, TertiarySequence Homology, Amino AcidSodium ChannelsTransfectionConceptsSegments S5Point mutationsS5 segmentVoltage-Gated Sodium ChannelSodium channelsTransmembrane segments S5Cytoplasmic interfaceWild-type channelsParalysis phenotypeHomologous domainsVoltage-sensitive sodium channelsPotassium-aggravated myotoniaNew point mutationPhenylalanine substitutionSkeletal muscle disordersHyperkalaemic periodic paralysisFast inactivationSecond domainMutationsGenesChannel deactivationInactivationChannel activationSlow inactivationT704M mutationDifferential role of GDNF and NGF in the maintenance of two TTX-resistant sodium channels in adult DRG neurons
Fjell J, Cummins T, Dib-Hajj S, Fried K, Black J, Waxman S. Differential role of GDNF and NGF in the maintenance of two TTX-resistant sodium channels in adult DRG neurons. Brain Research 1999, 67: 267-282. PMID: 10216225, DOI: 10.1016/s0169-328x(99)00070-4.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAxotomyCell SizeCell SurvivalDown-RegulationDrug ResistanceFemaleGanglia, SpinalGene ExpressionGlial Cell Line-Derived Neurotrophic FactorLectinsMembrane PotentialsNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelNerve Growth FactorsNerve Tissue ProteinsNeurons, AfferentNeuropeptidesPatch-Clamp TechniquesRatsRats, Sprague-DawleyRNA, MessengerSciatic NerveSodium ChannelsTetrodotoxinUp-RegulationConceptsTTX-R sodium currentsSNS/PN3Small DRG neuronsTTX-R currentsDRG neuronsIB4- neuronsSodium currentElectrophysiological propertiesSmall dorsal root ganglion neuronsDorsal root ganglion neuronsAxotomized DRG neuronsTTX-S currentsWhole-cell patch-clamp studiesTTX-resistant sodium channelsSciatic nerve transectionAdult DRG neuronsDifferent electrophysiological propertiesNear-normal levelsPatch-clamp studiesNerve transectionGDNF treatmentNeurotrophins NGFGanglion neuronsIsolectin IB4Exogenous NGFIn Vivo NGF Deprivation Reduces SNS Expression and TTX-R Sodium Currents in IB4-Negative DRG Neurons
Fjell J, Cummins T, Fried K, Black J, Waxman S. In Vivo NGF Deprivation Reduces SNS Expression and TTX-R Sodium Currents in IB4-Negative DRG Neurons. Journal Of Neurophysiology 1999, 81: 803-810. PMID: 10036280, DOI: 10.1152/jn.1999.81.2.803.Peer-Reviewed Original ResearchConceptsTTX-R sodium currentsNerve growth factorPA/pFDRG neuronsHigh antibody titersSodium current densityNGF-deprived neuronsSodium currentAntibody titersAdult ratsSmall dorsal root ganglion neuronsTetrodotoxin-resistant sodium channelsDorsal root ganglion neuronsTTX-R currentsSodium channel expressionMRNA hybridization signalsPathological painThermal hypoalgesiaGanglion neuronsControl neuronsIsolectin IB4Channel expressionNGF deprivationMRNA expressionNeurons
1998
Slow Closed-State Inactivation: A Novel Mechanism Underlying Ramp Currents in Cells Expressing the hNE/PN1 Sodium Channel
Cummins T, Howe J, Waxman S. Slow Closed-State Inactivation: A Novel Mechanism Underlying Ramp Currents in Cells Expressing the hNE/PN1 Sodium Channel. Journal Of Neuroscience 1998, 18: 9607-9619. PMID: 9822722, PMCID: PMC6793269, DOI: 10.1523/jneurosci.18-23-09607.1998.Peer-Reviewed Original ResearchConceptsTTX-S currentsRamp currentsDRG neuronsClosed-state inactivationSensory neuronsChannel isoformsDistinct integrative propertiesSmall DRG neuronsSodium channelsTTX-sensitive currentsSlow ramp depolarizationSteady-state inactivationRamp depolarizationNeuronsSkeletal muscleState inactivationIntegrative propertiesInactivation propertiesOpen-state inactivationExcitable cellsNovel mechanismCellsDepolarizationInactivationPN1SNS Na+ channel expression increases in dorsal root ganglion neurons in the carrageenan inflammatory pain model
Tanaka M, Cummins T, Ishikawa K, Dib-Hajj S, Black J, Waxman S. SNS Na+ channel expression increases in dorsal root ganglion neurons in the carrageenan inflammatory pain model. Neuroreport 1998, 9: 967-972. PMID: 9601651, DOI: 10.1097/00001756-199804200-00003.Peer-Reviewed Original ResearchConceptsSmall DRG neuronsDorsal root ganglion neuronsInjection of carrageenanDRG neuronsInflamed limbGanglion neuronsSodium currentTTX-R sodium currentsTetrodotoxin-resistant sodium currentInflammatory pain modelDevelopment of hyperexcitabilitySodium channel expressionPatch-clamp recordingsInflammatory painPain modelChronic painCarrageenan injectionNociceptive cellsContralateral sideNaive ratsChannel expressionProjection fieldsMRNA expressionNeuronsSodium channels
1997
Differential Effects of NGF and BDNF on Axotomy-Induced Changes in GABAA-Receptor-Mediated Conductance and Sodium Currents in Cutaneous Afferent Neurons
Oyelese A, Rizzo M, Waxman S, Kocsis J. Differential Effects of NGF and BDNF on Axotomy-Induced Changes in GABAA-Receptor-Mediated Conductance and Sodium Currents in Cutaneous Afferent Neurons. Journal Of Neurophysiology 1997, 78: 31-42. PMID: 9242258, PMCID: PMC2605357, DOI: 10.1152/jn.1997.78.1.31.Peer-Reviewed Original ResearchConceptsBrain-derived neurotrophic factorCutaneous afferent neuronsNerve growth factorReceptor-mediated conductanceProportion of neuronsAfferent neuronsAction potential waveformSodium currentNeurotrophic factorL4/L5 DRG neuronsAction potentialsVoltage-dependent sodium currentsWhole-cell patch-clamp techniqueDorsal root ganglion neuronsCell patch-clamp techniqueAxotomy-induced increaseFluoro-Gold injectionsL5 DRG neuronsSpecific neurotrophic factorsSciatic nerve stumpsTTX-sensitive currentsInjury-induced changesResistant sodium currentsGamma-aminobutyric acidPatch-clamp techniqueTTX-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 oligodeoxynucleotidesCordCellsTreatmentAction potential-like responses in B 104 cells with low Na+ channel densities
Gu X, Waxman S. Action potential-like responses in B 104 cells with low Na+ channel densities. Brain Research 1996, 735: 50-58. PMID: 8905169, DOI: 10.1016/0006-8993(96)00604-x.Peer-Reviewed Original ResearchConceptsAction potential-like responsesB104 cellsWhole-cell patch-clamp methodB104 neuroblastoma cellsPA/pFCurrent-clamp modeSteady-state inactivationAction potential generationPatch-clamp methodMicroM TTXNeuroblastoma cellsPrepulse potentialPotential generationResponse amplitudeCellsResponseStimuli
1995
Selective loss of slow and enhancement of fast Na+currents in cutaneous afferent dorsal root ganglion neurones following axotomy
Rizzo M, Kocsis J, Waxman S. Selective loss of slow and enhancement of fast Na+currents in cutaneous afferent dorsal root ganglion neurones following axotomy. Neurobiology Of Disease 1995, 2: 87-96. PMID: 8980012, DOI: 10.1006/nbdi.1995.0009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsFemaleGanglia, SpinalNeurons, AfferentPatch-Clamp TechniquesRatsRats, WistarSkinSodium Channels