2023
Sodium currents in naïve mouse dorsal root ganglion neurons: No major differences between sexes
Ghovanloo M, Tyagi S, Zhao P, Effraim P, Dib-Hajj S, Waxman S. Sodium currents in naïve mouse dorsal root ganglion neurons: No major differences between sexes. Channels 2023, 18: 2289256. PMID: 38055732, PMCID: PMC10761158, DOI: 10.1080/19336950.2023.2289256.Peer-Reviewed Original ResearchConceptsSexual dimorphismRodent dorsal root ganglion neuronsBiophysical propertiesDorsal root ganglion neuronsExpression patternsSex-dependent regulationVoltage-gated sodiumFunctional analysisGanglion neuronsRodent sensory neuronsMouse dorsal root ganglion neuronsNaïve WT miceNumber of cellsMixed populationDimorphismUniform experimental conditionsSex-dependent differencesSensory neuronsNative DRG neuronsPain pathwaysDRG neuronsWT miceClinical studiesNav currentsAdult malesNav1.7 gain-of-function mutation I228M triggers age-dependent nociceptive insensitivity and C-LTMR dysregulation
Wimalasena N, Taub D, Shim J, Hakim S, Kawaguchi R, Chen L, El-Rifai M, Geschwind D, Dib-Hajj S, Waxman S, Woolf C. Nav1.7 gain-of-function mutation I228M triggers age-dependent nociceptive insensitivity and C-LTMR dysregulation. Experimental Neurology 2023, 364: 114393. PMID: 37003485, PMCID: PMC10171359, DOI: 10.1016/j.expneurol.2023.114393.Peer-Reviewed Original ResearchConceptsParoxysmal extreme pain disorderSmall fiber neuropathyFunction mutationsDRG neuron hyperexcitabilityYoung adult miceVoltage-gated sodium channel NaSodium conductanceAge-related changesNeuron hyperexcitabilityPain disordersCongenital insensitivitySodium channel NaExcitability changesFemale miceMouse DRGYoung miceNeuronal excitabilityNoxious heatSkin lesionsVoltage-gated channelsAdult miceNeuron subtypesNervous systemProfound insensitivityMice
2020
Cumulative hydropathic topology of a voltage‐gated sodium channel at atomic resolution
Xenakis M, Kapetis D, Yang Y, Heijman J, Waxman S, Lauria G, Faber C, Smeets H, Westra R, Lindsey P. Cumulative hydropathic topology of a voltage‐gated sodium channel at atomic resolution. Proteins Structure Function And Bioinformatics 2020, 88: 1319-1328. PMID: 32447794, DOI: 10.1002/prot.25951.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceArcobacterBacterial ProteinsBinding SitesHydrophobic and Hydrophilic InteractionsIon Channel GatingModels, MolecularProtein BindingProtein Conformation, alpha-HelicalProtein Conformation, beta-StrandProtein Interaction Domains and MotifsSodiumThermodynamicsVoltage-Gated Sodium ChannelsConceptsVoltage-gated sodium channelsBacterial channelsPhysiological cellular activitySodium channelsCellular activitiesCell membraneBiological poresPore stabilityAtomic resolutionBiophysical significanceMembrane surfaceHydropathicityGenesProteinMutationsWide spectrumMembraneFunctional architectureAccumulationComputational frameworkSodium ionsPores
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
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
1999
In 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
Effects of Glucose Deprivation, Chemical Hypoxia, and Simulated Ischemia on Na+ Homeostasis in Rat Spinal Cord Astrocytes
Rose C, Waxman S, Ransom B. Effects of Glucose Deprivation, Chemical Hypoxia, and Simulated Ischemia on Na+ Homeostasis in Rat Spinal Cord Astrocytes. Journal Of Neuroscience 1998, 18: 3554-3562. PMID: 9570787, PMCID: PMC6793162, DOI: 10.1523/jneurosci.18-10-03554.1998.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornAntimetabolitesAstrocytesBenzofuransCell HypoxiaDeoxyglucoseEnergy MetabolismEnzyme InhibitorsEthers, CyclicExcitatory Amino Acid AgonistsFluorescent DyesFluorides, TopicalGlucoseGlycolysisHomeostasisIschemiaKainic AcidNeurotoxinsOuabainRatsRats, Sprague-DawleySodiumSodium AzideSodium FluorideSodium-Potassium-Exchanging ATPaseSpinal CordTetrodotoxinConceptsSpinal cord astrocytesChemical hypoxiaGlucose deprivationEnergy failureCultured spinal cord astrocytesGlutamatergic agonist kainateGlucose salineGlutamate reuptakeVivo ischemiaSpinal cordGlial functionMetabolic insultsSimulated ischemiaAgonist kainateIschemiaStandard salineAstrocytesSalineHypoxiaIntracellular ion concentrationsGlucose removalExtracellular spaceDeprivationL-lactateReperfusion
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 activityInactivationBaseline
1994
Astrocyte 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
1992
Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger
Stys P, Waxman S, Ransom B. Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger. Journal Of Neuroscience 1992, 12: 430-439. PMID: 1311030, PMCID: PMC6575619, DOI: 10.1523/jneurosci.12-02-00430.1992.Peer-Reviewed Original ResearchConceptsRat optic nerveCompound action potentialAnoxic injuryOptic nerveWhite matterAction potentialsCentral white matter tractsWhite matter injuryCNS white matterMembrane depolarizationAnoxia/ischemiaWhite matter tractsCNS protectionAnoxic insultMyelinated tractsChannel blockersExchanger blockerIrreversible injuryExtracellular Ca2Mammalian CNSNerveInjuryMore injuriesBlockersFunctional integrityChapter 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
1991
Reverse Operation of the Na+ ‐Ca2+ Exchanger Mediates Ca 2+ Influx during Anoxia in Mammalian CNS White Mattera
STYS P, WAXMAN S, RANSOM B. Reverse Operation of the Na+ ‐Ca2+ Exchanger Mediates Ca 2+ Influx during Anoxia in Mammalian CNS White Mattera. Annals Of The New York Academy Of Sciences 1991, 639: 328-332. PMID: 1785859, DOI: 10.1111/j.1749-6632.1991.tb17321.x.Peer-Reviewed Original Research
1987
Chapter 8 Ionic channel organization of normal and regenerating mammalian axons
Kocsis J, Waxman S. Chapter 8 Ionic channel organization of normal and regenerating mammalian axons. Progress In Brain Research 1987, 71: 89-101. PMID: 2438722, DOI: 10.1016/s0079-6123(08)61816-6.Peer-Reviewed Original ResearchConceptsNerve fibersPeripheral nervesRegenerated nerve fibersCell remodellingNormal developmentMammalian nerve fibresSchwann cellsElectrophysiological characteristicsFine caliberMyelinated axonsImmature axonsAxonal growthMammalian axonsNerveNormal maturationRemodelling occursAxonsCell arrestRemodellingTime courseMyelinIonic channelsLong termMaturationTime of maturation
1986
Differences in intramembranous particle distribution in the paranodal axolemma are not associated with functional differences of dorsal and ventral roots
Fields R, Black J, Bowe C, Kocsis J, Waxman S. Differences in intramembranous particle distribution in the paranodal axolemma are not associated with functional differences of dorsal and ventral roots. Neuroscience Letters 1986, 67: 13-18. PMID: 2425295, DOI: 10.1016/0304-3940(86)90200-4.Peer-Reviewed Original Research
1985
Organization of Ion Channels in the Myelinated Nerve Fiber
Waxman S, Ritchie J. Organization of Ion Channels in the Myelinated Nerve Fiber. Science 1985, 228: 1502-1507. PMID: 2409596, DOI: 10.1126/science.2409596.Peer-Reviewed Original Research
1982
Rat optic nerve: Electrophysiological, pharmacological and anatomical studies during development
Foster R, Connors B, Waxman S. Rat optic nerve: Electrophysiological, pharmacological and anatomical studies during development. Brain Research 1982, 3: 371-386. PMID: 7066695, DOI: 10.1016/0165-3806(82)90005-0.Peer-Reviewed Original ResearchConceptsCompound action potentialAction potentialsConduction velocityOptic nerveOptic nerve axonsShort latency peaksRat optic nerveAxonal membrane propertiesShort-latency componentsSixth postnatal dayOnset of myelinationWeeks of ageRelative refractory periodDays of ageGlial cellsPostnatal dayRefractory periodNerve axonsAxonal diameterLatency componentsCalcium conductanceAxonal sizeMyelinationNerve growthLatency peaks
1981
Basic and clinical electrophysiology of demyelinating diseases.
Ritchie J, Waxman S, Waksman B. Basic and clinical electrophysiology of demyelinating diseases. Neurology 1981, 31: 1308-10. PMID: 6287348, DOI: 10.1212/wnl.31.10.1308.Peer-Reviewed Original Research
1980
Ionic channel distribution and heterogeneity of the axon membrane in myelinated fibers.
Waxman S, Foster R. Ionic channel distribution and heterogeneity of the axon membrane in myelinated fibers. Brain Research 1980, 203: 205-34. PMID: 6253027, DOI: 10.1016/0165-0173(80)90008-9.Peer-Reviewed Original Research