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
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