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- Title
A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis.
- Authors
Shields, Shannon D; Cheng, Xiaoyang; Gasser, Andreas; Saab, Carl Y; Tyrrell, Lynda; Eastman, Emmanuella M; Iwata, Masashi; Zwinger, Pamela J; Black, Joel A; Dib-Hajj, Sulayman D; Waxman, Stephen G
- Abstract
Cerebellar dysfunction in multiple sclerosis (MS) contributes significantly to disability, is relatively refractory to symptomatic therapy, and often progresses despite treatment with disease-modifying agents. We previously observed that sodium channel Nav1.8, whose expression is normally restricted to the peripheral nervous system, is present in cerebellar Purkinje neurons in a mouse model of MS (experimental autoimmune encephalomyelitis [EAE]) and in humans with MS. Here, we tested the hypothesis that upregulation of Nav1.8 in cerebellum in MS and EAE has functional consequences contributing to symptom burden.
- Publication
Annals of neurology, 2012, Vol 71, Issue 2, p186
- ISSN
1531-8249
- Publication type
Journal Article
- DOI
10.1002/ana.22665