2021
Contributions of NaV1.8 and NaV1.9 to excitability in human induced pluripotent stem-cell derived somatosensory neurons
Alsaloum M, Labau JIR, Liu S, Estacion M, Zhao P, Dib-Hajj F, Waxman SG. Contributions of NaV1.8 and NaV1.9 to excitability in human induced pluripotent stem-cell derived somatosensory neurons. Scientific Reports 2021, 11: 24283. PMID: 34930944, PMCID: PMC8688473, DOI: 10.1038/s41598-021-03608-x.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAutopsyCell DifferentiationElectrophysiologyHumansImmunohistochemistryInduced Pluripotent Stem CellsMembrane PotentialsMutationNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelNeuronsNeurosciencesPainPatch-Clamp TechniquesProtein IsoformsSensory Receptor CellsSomatosensory CortexConceptsNeuronal excitabilitySomatosensory neuronsPluripotent stem cell-derived sensory neuronsDynamic clamp electrophysiologyTreatment of painPromising novel modalityVoltage-gated sodium channelsSodium channel isoformsNeuronal membrane potentialGenetic knockout modelsNav1.9 currentsPharmacologic blockSensory neuronsNav1.8Cellular correlatesRepetitive firingClamp electrophysiologyExcitabilityNeuronal backgroundNovel modalityChannel isoformsSodium channelsNeuronsNav1.9Knockout models
2020
Cannabidiol protects against high glucose‐induced oxidative stress and cytotoxicity in cardiac voltage‐gated sodium channels
Fouda MA, Ghovanloo M, Ruben PC. Cannabidiol protects against high glucose‐induced oxidative stress and cytotoxicity in cardiac voltage‐gated sodium channels. British Journal Of Pharmacology 2020, 177: 2932-2946. PMID: 32077098, PMCID: PMC7279989, DOI: 10.1111/bph.15020.Peer-Reviewed Original ResearchConceptsHigh glucoseOxidative stressHigh glucose-induced oxidative stressCardiac voltage-gated sodium channelGlucose-induced oxidative stressReactive oxygen speciesCardiac sodium channel isoformChannel inhibitory effectVoltage-gated sodium channelsSteady-state fast inactivationHigh glucose conditionsSodium channel isoformsAction potential modellingDeleterious effectsCardiovascular complicationsDiabetic patientsAction potentialsCell viability assaysArrhythmiasMajor causeInhibitory effectChannel isoformsCannabidiolGlucose conditionsSodium channels
2017
Tuning Neuronal Potassium Channels to the Auditory Environment
Kaczmarek L. Tuning Neuronal Potassium Channels to the Auditory Environment. Springer Handbook Of Auditory Research 2017, 64: 133-159. DOI: 10.1007/978-3-319-21530-3_6.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsBrainstem nucleiPotassium channelsAuditory brainstem nucleiVoltage-dependent potassium channelsNeuronal potassium channelsAuditory discrimination taskAuditory neuronsAuditory environmentChannel isoformsNeuronsHigh rateAuditory informationKv3.1Molecular mechanismsDifferent auditory environmentsRapid alterationsDiscrimination task
2011
Sodium channels and microglial function
Black JA, Waxman SG. Sodium channels and microglial function. Experimental Neurology 2011, 234: 302-315. PMID: 21985863, DOI: 10.1016/j.expneurol.2011.09.030.Peer-Reviewed Original ResearchConceptsCentral nervous systemSodium channel isoformsEffector functionsChannel isoformsMultiple cytokines/chemokinesResident immune cellsResponse of microgliaCytokines/chemokinesVoltage-gated sodium channel isoformsSpinal cord parenchymaSodium channel activityMicroglial functionPromotion of repairCord parenchymaImmune cellsMicrogliaNervous systemCell surface receptorsContinuous surveillanceAdhesion moleculesSodium channelsActivating signalsChannel activitySignaling pathwaysSurface receptors
2010
A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons
Estacion M, Gasser A, Dib-Hajj SD, Waxman SG. A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons. Experimental Neurology 2010, 224: 362-368. PMID: 20420834, DOI: 10.1016/j.expneurol.2010.04.012.Peer-Reviewed Original ResearchConceptsHippocampal neuronsCardiac muscle sodium channelsCryptogenic partial epilepsyHippocampal neuron excitabilitySodium channelsSomatic pain disordersDifferent sodium channel isoformsHuman chromosome 2Sodium channel isoformsPain disordersPartial epilepsyNeuron excitabilityPathophysiological basisExcitability disordersSpontaneous firingSodium channel mutationsGene SCN1ASodium channelopathiesCharge-neutralizing mutationsRamp currentsMuscle sodium channelsChromosome 2Channel isoformsChannel mutationsFunctional analysis
2009
Dorsal Root Ganglion Neurons
Rush A, Waxman S. Dorsal Root Ganglion Neurons. 2009, 615-619. DOI: 10.1016/b978-008045046-9.01660-0.Peer-Reviewed Original Research
2008
Multiple sodium channel isoforms and mitogen‐activated protein kinases are present in painful human neuromas
Black JA, Nikolajsen L, Kroner K, Jensen TS, Waxman SG. Multiple sodium channel isoforms and mitogen‐activated protein kinases are present in painful human neuromas. Annals Of Neurology 2008, 64: 644-653. PMID: 19107992, DOI: 10.1002/ana.21527.Peer-Reviewed Original ResearchConceptsMultiple sodium channel isoformsHuman neuromasSodium channel isoformsPainful neuromasMitogen-activated protein kinaseERK1/2 MAP kinasesNeuronal voltage-gated sodium channelsChannel isoformsSodium channel Nav1.3Sodium channelsSpontaneous ectopic dischargeTreatment of painSodium channel Nav1.1Possible therapeutic targetVoltage-gated sodium channelsMAP kinase p38Ectopic dischargesChronic painTraumatic neuromaChannel Nav1.1MAP kinaseExtracellular signal-regulated kinases 1NeuromaTherapeutic targetPain
2007
Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons
Rush AM, Cummins TR, Waxman SG. Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons. The Journal Of Physiology 2007, 579: 1-14. PMID: 17158175, PMCID: PMC2075388, DOI: 10.1113/jphysiol.2006.121483.Peer-Reviewed Original ResearchConceptsSodium channel isoformsDorsal root ganglion neuronsChannel isoformsDRG neuronsGanglion neuronsSpecific sodium channel isoformsMultiple sodium channelsSodium channelsPattern of expressionModulatory moleculesDisease insultsModulation of channelsPlasticity of expressionNeuronsDifferent subclassesExcitabilityDistinct biophysical characteristicsIsoformsExpressionBody of literatureInsultImportant roleResponse
2006
Axonal conduction and injury in multiple sclerosis: the role of sodium channels
Waxman SG. Axonal conduction and injury in multiple sclerosis: the role of sodium channels. Nature Reviews Neuroscience 2006, 7: 932-941. PMID: 17115075, DOI: 10.1038/nrn2023.Peer-Reviewed Original ResearchConceptsAxonal degenerationSodium channelsChannel isoformsDistinct pathophysiological rolesKey PointsMultiple sclerosisMultiple neurological deficitsRelapsing-remitting courseRestoration of conductionDegeneration of axonsCerebellar Purkinje neuronsVoltage-gated sodium channelsContext of demyelinationNeurological deficitsProgressive courseMultiple sclerosisAxonal conductionDisease progressionNav1.8 channelsConduction failurePathophysiological rolePurkinje neuronsCNS axonsFiring patternsLoss of coordinationAberrant expression
2005
Contactin regulates the current density and axonal expression of tetrodotoxin‐resistant but not tetrodotoxin‐sensitive sodium channels in DRG neurons
Rush AM, Craner MJ, Kageyama T, Dib‐Hajj S, Waxman SG, Ranscht B. Contactin regulates the current density and axonal expression of tetrodotoxin‐resistant but not tetrodotoxin‐sensitive sodium channels in DRG neurons. European Journal Of Neuroscience 2005, 22: 39-49. PMID: 16029194, DOI: 10.1111/j.1460-9568.2005.04186.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsCell Adhesion Molecules, NeuronalCell MembraneCells, CulturedContactinsDown-RegulationGanglia, SpinalMembrane PotentialsMiceMice, Inbred C57BLMice, KnockoutNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelNerve Fibers, UnmyelinatedNeurons, AfferentNeuropeptidesNociceptorsPatch-Clamp TechniquesPlant LectinsSodium Channel BlockersSodium ChannelsTetrodotoxinConceptsTTX-S channelsDRG neuronsSodium channelsSmall-diameter dorsal root ganglion neuronsSmall-diameter DRG neuronsWhole-cell patch-clamp recordingsTetrodotoxin-sensitive sodium channelsDorsal root ganglion neuronsChannel isoformsNociceptive DRG neuronsTTX-sensitive sodium channelsSodium channel Nav1.2Patch-clamp recordingsSodium channel isoformsPositive neuronsGanglion neuronsSciatic nerveCell surface expressionIsolectin B4Axonal expressionUnmyelinated axonsMammalian neuronal cellsLitter matesNav1.9Neuronal cells
2003
Modulation of the Kv3.1b Potassium Channel Isoform Adjusts the Fidelity of the Firing Pattern of Auditory Neurons
Macica CM, von Hehn CA, Wang LY, Ho CS, Yokoyama S, Joho RH, Kaczmarek LK. Modulation of the Kv3.1b Potassium Channel Isoform Adjusts the Fidelity of the Firing Pattern of Auditory Neurons. Journal Of Neuroscience 2003, 23: 1133-1141. PMID: 12598601, PMCID: PMC6742259, DOI: 10.1523/jneurosci.23-04-01133.2003.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsBrain StemCells, CulturedCHO CellsCricetinaeElectric ConductivityEvoked Potentials, AuditoryKineticsMiceMice, KnockoutNeuronsNeuropeptidesPatch-Clamp TechniquesPhosphorylationPotassium ChannelsPotassium Channels, Voltage-GatedProtein IsoformsProtein Kinase CSerineShaw Potassium ChannelsTetradecanoylphorbol AcetateConceptsTrapezoid bodyMedial nucleusAuditory neuronsHigh-frequency stimulationWild-type neuronsKv3.1 potassium channelHigh-threshold componentPotassium channel isoformsGreat temporal precisionPartial decreaseProtein kinase C activationAction potentialsLocation of soundsMice resultsFiring patternsNeuronsSensory stimulationPotassium channelsChannel isoformsKinase C activationKv3.1Kv3.1 geneStimulationHigh frequencyProtein kinase C
2002
Critical Molecular Determinants of Voltage-Gated Sodium Channel Sensitivity to μ-Conotoxins GIIIA/B
Cummins T, Aglieco F, Dib-Hajj S. Critical Molecular Determinants of Voltage-Gated Sodium Channel Sensitivity to μ-Conotoxins GIIIA/B. Molecular Pharmacology 2002, 61: 1192-1201. DOI: 10.1016/s0026-895x(24)12216-x.Peer-Reviewed Original ResearchRat skeletal muscle sodium channelsSodium channel isoformsSkeletal muscle sodium channelMuscle sodium channelsBinding to specific residuesChannel isoformsNeuronal channelsSodium channelsHigh-affinity binding sitesRNav1.4Electrophysiological techniquesExchange of serineNav1.4K substitutionGIIIBDevelopment of toxinsHNav1.4Molecular determinantsPore residuesDifferential sensitivityChannel sensitivityChimera constructs
2000
Molecular Determinants of Hair Cell Phenotypic Heterogeneity—Differential Expression of K Channel Genes
Navaratnam D, Oberholtzer J. Molecular Determinants of Hair Cell Phenotypic Heterogeneity—Differential Expression of K Channel Genes. 2000, 55-68. DOI: 10.1007/978-1-4615-4223-0_4.Peer-Reviewed Original ResearchChannel genesGene expressionAuditory receptor epitheliumAdditional gene productsK channel genesBK channel variantsLevel of transcriptionHair cellsPotassium channel genesRNA processingAlternative splicingSingle geneGene productsReceptor hair cellsReceptor epitheliumExpression patternsComplex patternsGenesMolecular determinantsChannel variantsLarge familyChick basilar papillaPhenotypic heterogeneityBasilar papillaChannel isoforms
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 mechanismCellsDepolarizationInactivationPN1
1997
Differential Distribution of Ca2+-Activated K+ Channel Splice Variants among Hair Cells along the Tonotopic Axis of the Chick Cochlea
Navaratnam D, Bell T, Tu T, Cohen E, Oberholtzer J. Differential Distribution of Ca2+-Activated K+ Channel Splice Variants among Hair Cells along the Tonotopic Axis of the Chick Cochlea. Neuron 1997, 19: 1077-1085. PMID: 9390520, DOI: 10.1016/s0896-6273(00)80398-0.Peer-Reviewed Original Research
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