2002
HSV-1 Helper Virus 5dl1.2 Suppresses Sodium Currents in Amplicon-Transduced Neurons
White BH, Cummins TR, Wolf DH, Waxman SG, Russell DS, Kaczmarek LK. HSV-1 Helper Virus 5dl1.2 Suppresses Sodium Currents in Amplicon-Transduced Neurons. Journal Of Neurophysiology 2002, 87: 2149-2157. PMID: 11929932, DOI: 10.1152/jn.00498.2001.Peer-Reviewed Original ResearchConceptsSodium currentAnti-HSV antibodiesAverage spike frequencyWild-type HSV-1Helper virusViral-based strategiesDays of transductionCultured neuronsHSV-1Spike frequencyGene deliveryNeuronsMammalian neuronsAmplicon systemSimilar suppressionHSV-1 genesVirusTherapeutic purposesViral proteinsAmplicon preparationsCellsCoinfectionSuppressionPreparation resultsTitersNitric 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
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 gangliaDirect Interaction with Contactin Targets Voltage-gated Sodium Channel Nav1.9/NaN to the Cell Membrane*
Liu C, Dib-Hajj S, Black J, Greenwood J, Lian Z, Waxman S. Direct Interaction with Contactin Targets Voltage-gated Sodium Channel Nav1.9/NaN to the Cell Membrane*. Journal Of Biological Chemistry 2001, 276: 46553-46561. PMID: 11581273, DOI: 10.1074/jbc.m108699200.Peer-Reviewed Original ResearchConceptsDorsal root gangliaRoot gangliaSodium channelsSmall sensory neuronsVoltage-gated sodium channelsTrigeminal ganglionNerve endingsC-fibersSensory neuronsNeuron somataChinese hamster ovary cell lineDifferent physiological propertiesGangliaHamster ovary cell lineNeuronal membranesChinese hamster ovary cellsOvary cell lineProtein complexesSurface expressionHamster ovary cellsCell linesAxonsSurface localizationCell membraneOvary cellsβ1 adducin gene expression in DRG is developmentally regulated and is upregulated by glial-derived neurotrophic factor and nerve growth factor
Ghassemi F, Dib-Hajj S, Waxman S. β1 adducin gene expression in DRG is developmentally regulated and is upregulated by glial-derived neurotrophic factor and nerve growth factor. Brain Research 2001, 90: 118-124. PMID: 11406290, DOI: 10.1016/s0169-328x(01)00091-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalmodulin-Binding ProteinsCells, CulturedCytoskeletonGanglia, SpinalGene Expression ProfilingGene Expression Regulation, DevelopmentalGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorNerve Growth FactorsNerve Tissue ProteinsNeurons, AfferentNeuroprotective AgentsRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionConceptsGlial-derived neurotrophic factorReal-time reverse transcription-polymerase chain reactionNeurotrophic factorTrigeminal ganglionDRG culturesRat DRGGrowth factorDorsal root ganglion culturesAdult rat DRGRat dorsal root ganglion culturesSuperior cervical ganglionReverse transcription-polymerase chain reactionExpression levelsNerve growth factorNon-neural tissuesDRG tissueCervical ganglionSciatic nervePolymerase chain reactionGanglion culturesAdducin geneLevel of expressionGangliaLow expression levelsGene expression
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
Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain
Dib-Hajj S, Fjell J, Cummins TR, Zheng Z, Fried K, LaMotte R, Black JA, Waxman S. Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain. Pain 1999, 83: 591-600. PMID: 10568868, DOI: 10.1016/s0304-3959(99)00169-4.Peer-Reviewed Original ResearchConceptsTTX-R sodium channelsChronic constriction injury modelDRG neuronsSodium currentSodium channelsNeuropathic painInjury modelAxotomized dorsal root ganglion (DRG) neuronsSmall-diameter DRG neuronsTTX-R sodium currentsDorsal root ganglion neuronsTTX-S currentsSodium channel expressionGanglion neuronsSciatic nerveChannel expressionSodium channel transcriptsNeuronsNa currentPainChannel transcriptsSignificant changesLevels of transcriptsHyperalgesiaPrevious studiesSodium 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 ResearchConceptsNerve 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 mutation
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 mechanismCellsDepolarizationInactivationPN1Endogenous NMDA-Receptor Activation Regulates Glutamate Release in Cultured Spinal Neurons
Robert A, Black J, Waxman S. Endogenous NMDA-Receptor Activation Regulates Glutamate Release in Cultured Spinal Neurons. Journal Of Neurophysiology 1998, 80: 196-208. PMID: 9658041, DOI: 10.1152/jn.1998.80.1.196.Peer-Reviewed Original ResearchMeSH Keywords2-Amino-5-phosphonovalerate6-Cyano-7-nitroquinoxaline-2,3-dioneAnimalsAnimals, NewbornBicucullineCells, CulturedExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsGlutamic AcidNeuronsRatsRats, Sprague-DawleyReceptors, AMPAReceptors, N-Methyl-D-AspartateSpinal CordSynapsesTetrodotoxinTime FactorsConceptsAMPA excitatory postsynaptic currentsExcitatory postsynaptic currentsNMDA receptor activationCultured spinal neuronsNMDA receptorsSpinal neuronsPresynaptic terminalsNMDA receptor-mediated glutamatergic neurotransmissionSpontaneous excitatory postsynaptic currentsAspartate receptor activationNMDA receptor activityRelease of neurotransmittersNonsynaptic receptorsTTX applicationGlutamate releaseImmature neuronsGlutamatergic neurotransmissionPostsynaptic currentsSpinal cordReceptor activationReceptor activityQuantal sizeQuantal analysisCNS developmentElectrical activityNovel splice variants of the voltage-sensitive sodium channel alpha subunit
Oh Y, Waxman S. Novel splice variants of the voltage-sensitive sodium channel alpha subunit. Neuroreport 1998, 9: 1267-1272. PMID: 9631410, DOI: 10.1097/00001756-199805110-00002.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAmino Acid SequenceAnimalsAnimals, NewbornAstrocytesAstrocytomaBrainBucladesineCalcimycinCells, CulturedGenetic VariationMacromolecular SubstancesModels, MolecularMolecular Sequence DataPolymerase Chain ReactionProtein ConformationRatsRats, Sprague-DawleySodium ChannelsSpinal CordUp-RegulationConceptsChannel alpha subunitNeuroblastoma cellsSpinal cord astrocytesB104 neuroblastoma cellsCultured rat astrocytesChannel mRNA expressionNovel splice variantSplice variantsSodium channel alpha subunitAlpha-subunit mRNASpinal cordCerebral astrocytesUnique regulatory pathwaysAlpha subunitRat astrocytesAstrocytesMRNA expressionSubunit mRNAsMicroM A23187Dibutyryl cAMPPremature truncationCellsExpressionRegulatory pathwaysCordSNS 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 channelsMechanisms of enhancement of neurite regeneration in vitro following a conditioning sciatic nerve lesion
Lankford K, Waxman S, Kocsis J. Mechanisms of enhancement of neurite regeneration in vitro following a conditioning sciatic nerve lesion. The Journal Of Comparative Neurology 1998, 391: 11-29. PMID: 9527536, PMCID: PMC2605358, DOI: 10.1002/(sici)1096-9861(19980202)391:1<11::aid-cne2>3.0.co;2-u.Peer-Reviewed Original ResearchConceptsDorsal root gangliaConditioning lesionNerve injuryNerve regenerationAffected dorsal root ganglionControl dorsal root gangliaDenervated peripheral nervePrior nerve injurySciatic nerve lesionCultured DRG neuronsSciatic nerve transectionPeripheral target tissuesPeripheral nerve stumpRapid nerve regenerationAbility of neuronsSecond axotomyNerve lesionsDRG neuronsNerve transectionNerve stumpRoot gangliaControl neuronsPeripheral nervesNerve tractsAdult rats
1997
Pharmacological Characterization of Na+ Influx via Voltage-Gated Na+ Channels in Spinal Cord Astrocytes
Rose C, Ransom B, Waxman S. Pharmacological Characterization of Na+ Influx via Voltage-Gated Na+ Channels in Spinal Cord Astrocytes. Journal Of Neurophysiology 1997, 78: 3249-3258. PMID: 9405543, DOI: 10.1152/jn.1997.78.6.3249.Peer-Reviewed Original ResearchConceptsSpinal cordChannel inactivationCultured spinal cordSpinal cord astrocytesEffect of veratridineSodium-binding benzofuranMicroM tetrodotoxinPharmacological characterizationAgonist kainatePharmacological inhibitionTetrodotoxinAstrocytesVeratridineCordMembrane depolarizationKainateImportant functional roleInfluxFunctional roleInhibitionCellsProminent pathwayATPase activityInactivationBaselineRegulation of Na+ channel β1 and β2 subunit mRNA levels in cultured rat astrocytes
Oh Y, Lee Y, Waxman S. Regulation of Na+ channel β1 and β2 subunit mRNA levels in cultured rat astrocytes. Neuroscience Letters 1997, 234: 107-110. PMID: 9364509, DOI: 10.1016/s0304-3940(97)00694-0.Peer-Reviewed Original ResearchConceptsReverse transcription-polymerase chain reactionMRNA levelsSpinal cordCompetitive reverse transcription-polymerase chain reactionQuantitative competitive reverse transcription-polymerase chain reactionSpinal cord astrocytesRat optic nerveDibutyryl cAMPBeta 2 mRNACultured rat astrocytesTranscription-polymerase chain reactionBeta 1 mRNASubunit mRNA levelsNeuroblastoma cell linesOptic nerveChannel β1Cultured astrocytesRat astrocytesCalcium ionophoreAstrocytesBeta 1Chain reactionCell linesCordMRNANGF has opposing effects on Na+ channel III and SNS gene expression in spinal sensory neurons
Black J, Langworthy K, Hinson A, Dib-Hajj S, Waxman S. NGF has opposing effects on Na+ channel III and SNS gene expression in spinal sensory neurons. Neuroreport 1997, 8: 2331-2335. PMID: 9243635, DOI: 10.1097/00001756-199707070-00046.Peer-Reviewed Original ResearchConceptsNeurotrophin nerve growth factorSmall DRG neuronsExogenous NGFDRG neuronsDifferent sodium channel genesSmall dorsal root ganglion neuronsDorsal root ganglion neuronsSciatic nerve transectionMRNA levelsSpinal sensory neuronsNerve growth factorNerve transectionDRG culturesGanglion neuronsAlpha-IIIAdult ratsSensory neuronsPeripheral targetsSodium channel transcriptsMRNA expressionMembrane excitabilityNeuronsGrowth factorRetrograde transportChannel transcripts
1995
Differential up-regulation of sodium channel α- and β1-subunit mRNAs in cultured embryonic DRG neurons following exposure to NGF
Zur K, Oh Y, Waxman S, Black J. Differential up-regulation of sodium channel α- and β1-subunit mRNAs in cultured embryonic DRG neurons following exposure to NGF. Brain Research 1995, 30: 97-105. PMID: 7609649, DOI: 10.1016/0169-328x(94)00283-k.Peer-Reviewed Original ResearchConceptsSodium channel alphaNerve growth factorChannel alphaDRG neuronsCultured embryonic DRG neuronsΒ1 subunit mRNAPattern of expressionDorsal root ganglion neuronsSodium channel subunitsEmbryonic DRG neuronsPresence of NGFSitu hybridization cytochemistryAbsence of NGFBeta 1 mRNABeta-subunit mRNANAG mRNAChannel subunitsDevelopment proceedsSodium channel αE16 embryosGanglion neuronsMRNAAlpha-IIIChannel αAlpha IIDifferential Na+ channel β1 subunit mRNA expression in stellate and flat astrocytes cultured from rat cortex and cerebellum: A combined in situ hybridization and immunocytochemistry study
Oh Y, Waxman S. Differential Na+ channel β1 subunit mRNA expression in stellate and flat astrocytes cultured from rat cortex and cerebellum: A combined in situ hybridization and immunocytochemistry study. Glia 1995, 13: 166-173. PMID: 7782102, DOI: 10.1002/glia.440130303.Peer-Reviewed Original ResearchConceptsGFAP-positive astrocytesRat brainChannel beta 1 subunit (Na beta 1) mRNAMRNA expressionBeta 1 mRNA expressionSubunit mRNA expressionBeta 1 mRNABeta 1 subunit mRNARat cortexGranule cellsStellate astrocytesRat astrocytesAstrocytesChannel mRNAImmunocytochemistry methodSubunit mRNAsImmunocytochemistry studiesCerebellumBrainMRNASitu hybridizationRecent studiesDifferential expressionExpressionCells
1994
Rat brain Na+ channel mRNAs in non‐excitable Schwann cells
Oh Y, Black J, Waxman S. Rat brain Na+ channel mRNAs in non‐excitable Schwann cells. FEBS Letters 1994, 350: 342-346. PMID: 8070590, DOI: 10.1016/0014-5793(94)00807-8.Peer-Reviewed Original Research