2019
NaV1.6 regulates excitability of mechanosensitive sensory neurons
Israel MR, Tanaka BS, Castro J, Thongyoo P, Robinson SD, Zhao P, Deuis JR, Craik DJ, Durek T, Brierley SM, Waxman SG, Dib‐Hajj S, Vetter I. NaV1.6 regulates excitability of mechanosensitive sensory neurons. The Journal Of Physiology 2019, 597: 3751-3768. PMID: 31087362, DOI: 10.1113/jp278148.Peer-Reviewed Original ResearchConceptsPeripheral sensory neuronsPeripheral nervous systemDorsal root ganglion neuronsSensory neuronsVoltage-gated sodium channelsGanglion neuronsSodium channelsLarge-diameter dorsal root ganglion neuronsTonic action potential firingWhole-cell patch-clamp recordingsMultiple voltage-gated sodium channelsIntra-plantar injectionMechanosensitive sensory neuronsVivo behavioral assessmentsAction potential firingChannel activationPatch-clamp recordingsPotential therapeutic targetMechanical stimuliΒ-scorpion toxinSodium channel isoformsPain pathwaysThermal allodyniaPain generationSensory afferentsRat NaV1.7 loss-of-function genetic model: Deficient nociceptive and neuropathic pain behavior with retained olfactory function and intra-epidermal nerve fibers
Grubinska B, Chen L, Alsaloum M, Rampal N, Matson D, Yang C, Taborn K, Zhang M, Youngblood B, Liu D, Galbreath E, Allred S, Lepherd M, Ferrando R, Kornecook T, Lehto S, Waxman S, Moyer B, Dib-Hajj S, Gingras J. Rat NaV1.7 loss-of-function genetic model: Deficient nociceptive and neuropathic pain behavior with retained olfactory function and intra-epidermal nerve fibers. Molecular Pain 2019, 15: 1744806919881846. PMID: 31550995, PMCID: PMC6831982, DOI: 10.1177/1744806919881846.Peer-Reviewed Original ResearchConceptsOlfactory functionNav1.7 proteinPain behaviorPain responseRat modelSmall-diameter dorsal root ganglion neuronsNormal intraepidermal nerve fibre densityIntraepidermal nerve fiber densityIntra-epidermal nerve fibersDorsal root ganglion neuronsNeuropathic pain behaviorsNeuropathic pain responsesSpinal nerve ligationNerve fiber densityDorsal root gangliaAction potential firingPeripheral nervous systemEarly postnatal developmentGenetic animal modelsNav1.7 lossNerve ligationPain targetsNeuropathic conditionsGanglion neuronsRoot ganglia
2012
Nav1.8 expression is not restricted to nociceptors in mouse peripheral nervous system
Shields SD, Ahn H, Yang Y, Han C, Seal RP, Wood JN, Waxman SG, Dib-Hajj S. Nav1.8 expression is not restricted to nociceptors in mouse peripheral nervous system. Pain 2012, 153: 2017-2030. PMID: 22703890, DOI: 10.1016/j.pain.2012.04.022.Peer-Reviewed Original ResearchConceptsPeripheral nervous systemSensory neuronsKnockout mouse phenotypesNervous systemDorsal root ganglion neuronsUnmyelinated sensory afferentsPrimary sensory neuronsLow-threshold mechanoreceptorsMouse peripheral nervous systemGene functionVoltage-gated sodium channelsConditional knockout miceCytoskeletal proteinsIdentity of neuronsNav1.8 expressionMolecular markersDRG neuronsVast diversitySensory afferentsCre miceGanglion neuronsMouse phenotypeNoxious stimuliAβ fibersKnockout miceA channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis
Shields SD, Cheng X, Gasser A, Saab CY, Tyrrell L, Eastman EM, Iwata M, Zwinger PJ, Black JA, Dib‐Hajj S, Waxman SG. A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis. Annals Of Neurology 2012, 71: 186-194. PMID: 22367990, DOI: 10.1002/ana.22665.Peer-Reviewed Original ResearchConceptsMultiple sclerosisCerebellar dysfunctionMouse modelPurkinje neuronsNervous systemNew transgenic mouse modelPurkinje neuron firingDisease-modifying agentsSodium channel Nav1.8Healthy nervous systemPeripheral nervous systemTransgenic mouse modelCerebellar Purkinje neuronsWild-type littermatesNav1.8 expressionNeurons altersSymptom burdenSymptomatic therapySymptom progressionNav1.8Electrophysiological propertiesNeuron firingDysfunctionEAEMotor behavior
2000
Sensory 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 patterns