2025
ENaC contributes to macrophage dysfunction in cystic fibrosis
Moran J, Pugh C, Brown N, Thomas A, Zhang S, McCauley E, Cephas A, Shrestha C, Partida-Sanchez S, Bai S, Bruscia E, Kopp B. ENaC contributes to macrophage dysfunction in cystic fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2025, 329: l61-l69. PMID: 40454714, PMCID: PMC12181047, DOI: 10.1152/ajplung.00009.2025.Peer-Reviewed Original ResearchConceptsCystic fibrosis transmembrane conductance regulatorCystic fibrosis transmembrane conductance regulator modulatorsMonocyte-derived macrophagesEpithelial sodium channelTransmembrane conductance regulatorCystic fibrosisImmune cellsProinflammatory cytokine productionENaC modulationENaC expressionConductance regulatorCystic fibrosis transmembrane conductance regulator inhibitionCytokine productionSodium channelsCF airway epithelial cellsReduced proinflammatory cytokine productionDecreased proinflammatory cytokine productionSodium channel expressionInfection controlTherapeutic targetAirway epithelial cellsIon channel dysfunctionReactive oxygen speciesIon channelsCFTR expression
2024
Human IPSC-Derived Microglia Sense and Dampen Hyperexcitability of Cortical Neurons Carrying the Epilepsy-Associated SCN2A-L1342P Mutation
Que Z, Olivero-Acosta M, Robinson M, Chen I, Zhang J, Wettschurack K, Wu J, Xiao T, Otterbacher C, Shankar V, Harlow H, Hong S, Zirkle B, Wang M, Cui N, Mandal P, Chen X, Deming B, Halurkar M, Zhao Y, Rochet J, Xu R, Brewster A, Wu L, Yuan C, Skarnes W, Yang Y. Human IPSC-Derived Microglia Sense and Dampen Hyperexcitability of Cortical Neurons Carrying the Epilepsy-Associated SCN2A-L1342P Mutation. Journal Of Neuroscience 2024, 45: e2027232024. PMID: 39557580, PMCID: PMC11735681, DOI: 10.1523/jneurosci.2027-23.2024.Peer-Reviewed Original ResearchNeuronal excitabilityHyperexcitable neuronsHuman microgliaCo-CultureVoltage-gated sodium channel NaV1.2Neuronal activityRepetitive action potential firingRodent models of seizuresBrain-resident immune cellsSodium channel expressionInfluence neuronal excitabilityAction potential firingHyperexcitability of cortical neuronsModulates neuronal excitabilityEpilepsy-causing mutationsSodium channel Nav1.2Resident immune cellsAbnormal neuronal activityPresence of microgliaSuppression of seizuresModulate neuronal activityDensity of sodium channelsModels of seizuresPresence of neuronsAxon initial segment
2010
Sodium channel expression and function in multiple sclerosis
Bangalore L, Black J, Carrithers M, Waxman S. Sodium channel expression and function in multiple sclerosis. 2010, 29-43. DOI: 10.1017/cbo9780511781698.005.Peer-Reviewed Original ResearchMultiple sclerosisRecovery of functionSodium channel expressionHealth care advisorsMechanisms of recoveryNeurorehabilitation programChannel expressionSpecific syndromesTherapeutic interventionsCare advisorsClinical rehabilitationEfficient therapySclerosisDisease mechanismsPatientsCliniciansNeurorehabilitationInterventionBasic scienceSocial participationPathophysiologySyndromeTherapyNeuroplasticity
2009
Voltage-Gated Sodium Channels: Therapeutic Targets for Pain
Dib-Hajj S, Black JA, Waxman SG. Voltage-Gated Sodium Channels: Therapeutic Targets for Pain. Pain Medicine 2009, 10: 1260-1269. PMID: 19818036, DOI: 10.1111/j.1526-4637.2009.00719.x.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsDifferent pain statesPain statesVoltage-gated sodium channelsPain syndromeTherapeutic targetParoxysmal extreme pain disorderFunction mutationsIsoform-specific blockersSodium channelsInflammatory pain conditionsDifferent pain syndromesTreatment of painDorsal root gangliaSodium channel expressionMajor medical needsSodium channel blockersSodium channel isoformsAmeliorate painPain conditionsPain disordersChronic painTreatment optionsRoot gangliaNociceptor neuronsChannel blockers
2003
Patterned electrical activity modulates sodium channel expression in sensory neurons
Klein JP, Tendi EA, Dib‐Hajj S, Fields RD, Waxman SG. Patterned electrical activity modulates sodium channel expression in sensory neurons. Journal Of Neuroscience Research 2003, 74: 192-198. PMID: 14515348, DOI: 10.1002/jnr.10768.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsCells, CulturedDown-RegulationElectric StimulationFetusGanglia, SpinalImmunohistochemistryMiceNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelNerve Growth FactorNerve Tissue ProteinsNeurons, AfferentNeuropeptidesPeripheral NervesPeripheral Nervous System DiseasesRNA, MessengerSodium ChannelsConceptsExpression of Nav1.3Sodium channel expressionNerve growth factorSensory neuronsChannel expressionDorsal root ganglion neuronsEctopic neuronal dischargesPatterned electrical activitySodium channel Nav1.3Development of hyperexcitabilityPeripheral nerve injuryMouse sensory neuronsNeuronal activity levelsSubtype-specific mannerQuantitative polymerase chain reactionNav1.9 mRNANeuropathic painNerve injuryGanglion neuronsNeurotrophic factorPolymerase chain reactionNeuronal dischargeNeuronal activityElectrical stimulationNav1.8
2002
Primary motor neurons fail to up‐regulate voltage‐gated sodium channel Nav1.3/brain type III following axotomy resulting from spinal cord injury
Hains B, Black J, Waxman S. Primary motor neurons fail to up‐regulate voltage‐gated sodium channel Nav1.3/brain type III following axotomy resulting from spinal cord injury. Journal Of Neuroscience Research 2002, 70: 546-552. PMID: 12404508, DOI: 10.1002/jnr.10402.Peer-Reviewed Original ResearchConceptsSpinal cord injuryUpper motor neuronsPrimary motor cortexDorsal root gangliaMotor neuronsCord injuryMotor cortexRat primary motor cortexDorsal column transectionIpsilateral DRG neuronsCortical motor neuronsSciatic nerve transectionTraumatic head injuryFacial motor neuronsSodium channel expressionPrimary motor neuronsVoltage-gated sodium channelsPeripheral axotomyDRG neuronsNerve transectionLayer VControl brainsHead injuryRoot gangliaSpinal cord
2000
Sodium channels and their genes: dynamic expression in the normal nervous system, dysregulation in disease states11Published on the World Wide Web on 15 August 2000.
Waxman S, Dib-Hajj S, Cummins T, Black J. Sodium channels and their genes: dynamic expression in the normal nervous system, dysregulation in disease states11Published on the World Wide Web on 15 August 2000. Brain Research 2000, 886: 5-14. PMID: 11119683, DOI: 10.1016/s0006-8993(00)02774-8.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsSodium channel gene expressionSodium channel geneChannel gene expressionChannel genesGene expressionPost-transcriptional levelNormal nervous systemSodium channel expressionSodium channelsChannel expressionMolecular plasticityGenesDynamic expressionCell membraneHypothalamic magnocellular neurosecretory neuronsDifferent repertoiresMultiple sclerosisNervous systemTherapeutic opportunitiesSodium channel subtypesExpressionElectrogenic propertiesRegulationChannel subtypesDysregulationSensory 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 patternsThe neuron as a dynamic electrogenic machine: modulation of sodiumchannel expression as a basis for functional plasticity in neurons
Waxman S. The neuron as a dynamic electrogenic machine: modulation of sodiumchannel expression as a basis for functional plasticity in neurons. Philosophical Transactions Of The Royal Society B Biological Sciences 2000, 355: 199-213. PMID: 10724456, PMCID: PMC1692729, DOI: 10.1098/rstb.2000.0559.Peer-Reviewed Original ResearchConceptsSodium channelsMammalian nervous systemSodium channel geneNervous systemDozen genesDistinct sodium channelsVoltage-gated sodium channelsGenesElectrogenic machineryNormal nervous systemSodium channel expressionFunctional plasticityMembrane of neuronsAction potential activityTranscriptionPathological insultsPhysiological inputsMost neuronsCrucial roleExpressionNeuronsFunctional propertiesElectroresponsive propertiesPotential activityMachinerySodium channels and the molecular pathophysiology of pain
Cummins T, Dib-Hajj S, Black J, Waxman S. Sodium channels and the molecular pathophysiology of pain. Progress In Brain Research 2000, 129: 3-19. PMID: 11098678, DOI: 10.1016/s0079-6123(00)29002-x.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsDorsal root gangliaTrigeminal neuronsSodium channelsAction potentialsDorsal root ganglion neuronsSpontaneous action potential activityMolecular pathophysiologyPrimary sensory neuronsPeripheral target tissuesAction potential activitySodium channel expressionChain of neuronsPathological burstingNerve injuryNociceptive pathwaysChronic painGanglion neuronsRoot gangliaSensory neuronsChannel expressionSomatosensory systemPainNeuronsTarget tissuesPathophysiologyVoltage-gated sodium channels and the molecular pathogenesis of pain: a review.
Waxman SG, Cummins TR, Dib-Hajj SD, Black JA. Voltage-gated sodium channels and the molecular pathogenesis of pain: a review. The Journal Of Rehabilitation Research And Development 2000, 37: 517-28. PMID: 11322150.Peer-Reviewed Original ResearchConceptsVoltage-gated sodium channelsDRG neuronsNervous systemSodium channelsDistinct voltage-gated sodium channelsAction potentialsSpinal sensory neuronsSodium channel expressionSpontaneous action potentialsDifferent sodium channelsSpecific sodium channelsUnderstanding of painHigh-frequency activityInflammatory painPain pathwaysChronic painNociceptive signalsPeripheral nervesSensory neuronsNew therapiesPainChannel expressionMolecular pathogenesisPharmacologic manipulationNeuron cell membrane
1999
Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain
DibHajj 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 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 activityPainThe molecular pathophysiology of pain: abnormal expression of sodium channel genes and its contributions to hyperexcitability of primary sensory neurons
Waxman S. The molecular pathophysiology of pain: abnormal expression of sodium channel genes and its contributions to hyperexcitability of primary sensory neurons. Pain 1999, 82: s133-s140. PMID: 10491982, DOI: 10.1016/s0304-3959(99)00147-5.Peer-Reviewed Original ResearchConceptsPrimary sensory neuronsSodium channel gene expressionChannel gene expressionSodium channel expressionDRG neuronsSensory neuronsSodium channelsAxonal injuryChannel expressionSmall dorsal root ganglion neuronsAbnormal expressionDorsal root ganglion neuronsMolecular pathophysiologySodium channel geneAbnormal burst activityMultiple sodium channelsSNS/PN3Inflammatory pain modelChannel genesDistinct sodium channelsSodium current expressionInflammatory painNerve injuryPain modelGanglion neuronsSodium 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 overexpressionChanges in expression of voltage‐gated potassium channels in dorsal root ganglion neurons following axotomy
Ishikawa K, Tanaka M, Black J, Waxman S. Changes in expression of voltage‐gated potassium channels in dorsal root ganglion neurons following axotomy. Muscle & Nerve 1999, 22: 502-507. PMID: 10204786, DOI: 10.1002/(sici)1097-4598(199904)22:4<502::aid-mus12>3.0.co;2-k.Peer-Reviewed Original ResearchConceptsDorsal root ganglion neuronsDRG neuronsVoltage-gated potassium channelsAxonal injuryGanglion neuronsPotassium channelsChannel expressionNormal DRG neuronsChronic pain syndromeSodium channel expressionSpectrum of subtypesVoltage-gated sodium channelsSpecific potassium channelsPain syndromeDRG cellsAdult ratsNervous systemAxotomyKv expressionNeuronsImmunocytochemical methodsMolecular correlatesElectrical excitabilitySodium channelsImmunoreactivityIn 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
Glial cells have heart: rH1 Na+ channel mRNA and protein in spinal cord astrocytes
Black JA, Dib‐Hajj S, Cohen S, Hinson AW, Waxman SG. Glial cells have heart: rH1 Na+ channel mRNA and protein in spinal cord astrocytes. Glia 1998, 23: 200-208. PMID: 9633805, DOI: 10.1002/(sici)1098-1136(199807)23:3<200::aid-glia3>3.0.co;2-8.Peer-Reviewed Original ResearchConceptsTTX-resistant currentStellate astrocytesSpinal cordCultured spinal cord astrocytesVoltage-sensitive sodium currentsChannel mRNASodium currentDorsal root ganglion neuronsSodium channel immunoreactivityRT-PCRSpinal cord astrocytesTTX-sensitive currentsIntact spinal cordSpinal cord culturesReverse transcription-polymerase chain reactionSodium channel mRNASodium channel expressionTranscription-polymerase chain reactionTTX-resistant channelsPolyclonal antibodiesChannel immunoreactivityP7 ratsGanglion neuronsPolymerase chain reactionChannel antibodiesSNS 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
Schwann cells modulate sodium channel expression in spinal sensory neurons in vitro
Hinson AW, Gu XQ, Dib‐Hajj S, Black JA, Waxman SG. Schwann cells modulate sodium channel expression in spinal sensory neurons in vitro. Glia 1997, 21: 339-349. PMID: 9419009, DOI: 10.1002/(sici)1098-1136(199712)21:4<339::aid-glia1>3.0.co;2-z.Peer-Reviewed Original ResearchConceptsDRG neuronsSC-conditioned mediumSodium channel alphaE15 ratsSodium channelsChannel alphaSodium channel immunoreactivitySpinal sensory neuronsBeta2 subunit mRNASodium channel mRNASodium channel expressionFunctional sodium channelsSodium current densityBeta-subunit mRNAChannel immunoreactivityBeta2 mRNASensory neuronsClamp recordingsChannel expressionChannel mRNAIsoform-specific riboprobesNeuronsBeta1RatsHybridization signals
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