2024
The evolution of patch-clamp electrophysiology: robotic, multiplex, and dynamic.
Ghovanloo M, Dib-Hajj S, Waxman S. The evolution of patch-clamp electrophysiology: robotic, multiplex, and dynamic. Molecular Pharmacology 2024 PMID: 39164111, DOI: 10.1124/molpharm.124.000954.Peer-Reviewed Original ResearchPatch-clamp techniquePatch-clamp electrophysiologyPatch clampVoltage- and current-clamp modesIon channelsContribution of ion channelsCurrent-clamp modePatch-clamp methodOhm's lawDynamic-clampGating mechanisms of ion channelsMuscle cellsCardiac excitabilityGold standardExcitable cellsReceptorsGate conductionElectrophysiologyNeuronsElectrogenesisSimultaneous recordingCellsHigh-throughput automated platformMechanisms of ion channelsGating mechanism
2023
High-throughput combined voltage-clamp/current-clamp analysis of freshly isolated neurons
Ghovanloo M, Tyagi S, Zhao P, Kiziltug E, Estacion M, Dib-Hajj S, Waxman S. High-throughput combined voltage-clamp/current-clamp analysis of freshly isolated neurons. Cell Reports Methods 2023, 3: 100385. PMID: 36814833, PMCID: PMC9939380, DOI: 10.1016/j.crmeth.2022.100385.Peer-Reviewed Original ResearchConceptsDorsal root ganglion neuronsCurrent-clamp recordingsCurrent-clamp analysisVoltage-gated sodium channelsPatch-clamp techniqueExcitable cellsGanglion neuronsElectrophysiological recordingsNeuronal cellsNeuronsGold standard methodologySodium channelsCellular levelRobotic instrumentsCellsDrug screeningSame cellsIntact tissueRecordings
2012
Myelin, Impulse Conduction, and the Pathophysiology of Demyelination
Bangalore L, Waxman S. Myelin, Impulse Conduction, and the Pathophysiology of Demyelination. 2012, 529-542. DOI: 10.1093/med/9780199794591.003.0042.Peer-Reviewed Original ResearchPathophysiology of demyelinationNormal brain functionMultiple sclerosisGlial cellsParkinson's diseaseNeurological diseasesAlzheimer's diseasePsychiatric conditionsImpulse conductionBrain functionDiseaseGliaNeuronsBasic biologyCell anatomyConcerted actionCellsDemyelinationSclerosisPathophysiologyStrokeCentral roleBrainMyelin
2008
Alarm or curse? The pain of neuroinflammation
Saab C, Waxman S, Hains B. Alarm or curse? The pain of neuroinflammation. Brain Research Reviews 2008, 58: 226-235. PMID: 18486228, DOI: 10.1016/j.brainresrev.2008.04.002.Peer-Reviewed Original ResearchConceptsImmune cellsExperimental spinal cord injuryContribution of microgliaNociceptive nervous systemPeripheral nerve injuryExposure of neuronsSpinal cord injuryDevelopment of pharmacotherapiesNeuropathic injuryNeuropathic painNerve injuryPainful behaviorChronic painNeuroexcitatory effectsCord injuryChronic activationNervous systemPainImmune systemInjuryIdentification of moleculesNeuronsFunctional consequencesCellsDetrimental consequences
2006
Transcriptional Channelopathies of the Nervous System
Waxman S. Transcriptional Channelopathies of the Nervous System. 2006 DOI: 10.1002/9780470015902.a0006086.Peer-Reviewed Original ResearchSodium channel geneChannel genesTranscriptional channelopathiesSodium channel gene expressionChannel gene expressionGene expressionPeripheral nerve injurySpinal sensory neuronsGenesDysregulated expressionNerve injuryMultiple sclerosisSensory neuronsNervous systemCerebellar functionRecent studiesExpressionChannelopathiesAbstract Recent studiesHyperexcitabilitySclerosisInjuryNeuronsCells
2002
Axotomy does not up-regulate expression of sodium channel Nav1.8 in Purkinje cells
Black J, Dusart I, Sotelo C, Waxman S. Axotomy does not up-regulate expression of sodium channel Nav1.8 in Purkinje cells. Brain Research 2002, 101: 126-131. PMID: 12007840, DOI: 10.1016/s0169-328x(02)00200-0.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsAxotomyCerebellumDisease Models, AnimalFemaleGanglia, SpinalGene Expression RegulationImmunohistochemistryMultiple SclerosisNAV1.8 Voltage-Gated Sodium ChannelNeurons, AfferentNeuropeptidesPurkinje CellsRatsRats, WistarRNA, MessengerSodium ChannelsUp-RegulationZebrafish ProteinsConceptsMultiple sclerosisPurkinje cellsSensory neuron-specific sodium channelsDorsal root ganglion neuronsAberrant expressionSodium channelsHuman multiple sclerosisPrimary sensory neuronsSodium channel Nav1.8Specific sodium channelsCerebellar Purkinje cellsGanglion neuronsSensory neuronsAxotomySurgical modelSodium channel transcriptsExperimental modelCerebellar functionChannel transcriptsNeuronsSitu hybridizationCellsExpressionNav1.8SclerosisHSV-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 resultsTiters
2001
Acquired channelopathies in nerve injury and MS
Waxman S. Acquired channelopathies in nerve injury and MS. Neurology 2001, 56: 1621-1627. PMID: 11428390, DOI: 10.1212/wnl.56.12.1621.Peer-Reviewed Original ResearchConceptsNerve injurySodium channelsSensory neuron-specific sodium channelsSodium channel geneChannel genesPeripheral nerve injurySpinal sensory neuronsPathophysiology of MSSubtype-specific drugsDistinct sodium channelsVoltage-gated sodium channelsSpecific sodium channelsAxonal transectionGenetic channelopathyPrototype disorderSensory neuronsPurkinje cellsTherapeutic opportunitiesChannelopathiesAbnormal expressionInjuryMolecular changesHyperexcitabilityCellsTransection
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 mechanismCellsDepolarizationInactivationPN1Novel 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 pathwaysCord
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 activityInactivationBaselineDownregulation of Na+ channel mRNA in olfactory bulb tufted cells following deafferentiation
Sashihara S, Waxman S, Greer C. Downregulation of Na+ channel mRNA in olfactory bulb tufted cells following deafferentiation. Neuroreport 1997, 8: 1289-1293. PMID: 9175131, DOI: 10.1097/00001756-199703240-00046.Peer-Reviewed Original ResearchConceptsOlfactory bulbMitral cellsEffects of deafferentationPostnatal day 2Olfactory receptor cellsFunctional deafferentationAfferent inputChannel expressionDay 2Channel mRNAReceptor cellsChannel subunitsDeafferentationI mRNACauterizationCritical periodDetectable changeAlpha IIOdorant accessSitu hybridizationCellsCell propertiesExpressionBulbMRNA
1996
Orphan nuclear receptor RORα gene: isoform-specific spatiotemporal expression during postnatal development of brain
Sashihara S, Felts P, Waxman S, Matsui T. Orphan nuclear receptor RORα gene: isoform-specific spatiotemporal expression during postnatal development of brain. Brain Research 1996, 42: 109-117. PMID: 8915586, DOI: 10.1016/s0169-328x(96)00118-0.Peer-Reviewed Original ResearchConceptsROR alphaAlpha cDNAOrphan nuclear receptor ROR alphaSpatiotemporal expressionN-terminal regionIsoform-specific regulationAlpha expressionSpecific transcriptsCell typesHybridization signalsPurkinje cellsCDNAExpressionPostnatal developmentRelative levelsRegulationCellsAlphaPostnatal maturationTranscriptsOlfactory bulbRodent brainIsoformsBrain regionsMaturationManipulation 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 amplitudeCellsResponseStimuliVoltage-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 ResearchExpression of mRNA for a sodium channel in subfamily 2 in spinal sensory neurons
Waxman S, Black J. Expression of mRNA for a sodium channel in subfamily 2 in spinal sensory neurons. Neurochemical Research 1996, 21: 395-401. PMID: 8734431, DOI: 10.1007/bf02527702.Peer-Reviewed Original ResearchConceptsDorsal root gangliaSpinal sensory neuronsSchwann cellsDRG neuronsSensory neuronsRat dorsal root gangliaSodium channelsΒ1 subunitExpression of mRNARoot gangliaSpinal cordSitu hybridization cytochemistryNeuronsΑ-subunitAntisense riboprobesBlot analysisType IMRNACellsExpressionHigh levelsGangliaRNA blot analysisHippocampusCord
1995
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
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
1991
Na+‐Ca2+ exchanger mediates Ca2+ influx during anoxia in mammalian central nervous system white matter
Stys P, Waxman S, Ransom B. Na+‐Ca2+ exchanger mediates Ca2+ influx during anoxia in mammalian central nervous system white matter. Annals Of Neurology 1991, 30: 375-380. PMID: 1952825, DOI: 10.1002/ana.410300309.Peer-Reviewed Original ResearchConceptsWhite matterIsolated rat optic nerveCentral nervous system white matterNervous system white matterWhite matter injuryRat optic nerveMammalian central nervous systemSevere neurological impairmentCompound action potentialType of injuryCentral nervous systemFunctional recoveryOptic nervePharmacological blockadeNeurological impairmentAnoxic injuryIrreversible injuryNervous systemAction potentialsInjuryInfluxCa2Critical mechanismCellsNerve