2012
A 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
Sodium 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 StatementsMeSH KeywordsAnimalsDisease Models, AnimalGanglia, SpinalHumansInflammationNerve Growth FactorsNeuronsPainSodium ChannelsConceptsDorsal 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 tissuesPathophysiology