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A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis.

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A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis. / 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.

In: ANN NEUROL, Vol. 71, No. 2, 2, 2012, p. 186-194.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Shields, SD, Cheng, X, Gasser, A, Saab, CY, Tyrrell, L, Eastman, EM, Iwata, M, Zwinger, PJ, Black, JA, Dib-Hajj, SD & Waxman, SG 2012, 'A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis.', ANN NEUROL, vol. 71, no. 2, 2, pp. 186-194. <http://www.ncbi.nlm.nih.gov/pubmed/22367990?dopt=Citation>

APA

Shields, S. D., Cheng, X., Gasser, A., Saab, C. Y., Tyrrell, L., Eastman, E. M., Iwata, M., Zwinger, P. J., Black, J. A., Dib-Hajj, S. D., & Waxman, S. G. (2012). A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis. ANN NEUROL, 71(2), 186-194. [2]. http://www.ncbi.nlm.nih.gov/pubmed/22367990?dopt=Citation

Vancouver

Shields SD, Cheng X, Gasser A, Saab CY, Tyrrell L, Eastman EM et al. A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis. ANN NEUROL. 2012;71(2):186-194. 2.

Bibtex

@article{681f4f5cfc9e4d4f931997abdc575173,
title = "A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis.",
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.",
keywords = "Animals, Disease Models, Animal, Mice, Mice, Transgenic, Up-Regulation/genetics, Aniline Compounds/therapeutic use, Cerebellar Diseases/genetics/*physiopathology, Cerebellum/cytology/metabolism/pathology, Channelopathies/genetics/*physiopathology, Encephalomyelitis, Autoimmune, Experimental/drug therapy/*physiopathology, Furans/therapeutic use, Multiple Sclerosis/genetics/*physiopathology, NAV1.8 Voltage-Gated Sodium Channel, Purkinje Cells/pathology/physiology, Sodium Channel Blockers/therapeutic use, Sodium Channels/biosynthesis/genetics/metabolism, Animals, Disease Models, Animal, Mice, Mice, Transgenic, Up-Regulation/genetics, Aniline Compounds/therapeutic use, Cerebellar Diseases/genetics/*physiopathology, Cerebellum/cytology/metabolism/pathology, Channelopathies/genetics/*physiopathology, Encephalomyelitis, Autoimmune, Experimental/drug therapy/*physiopathology, Furans/therapeutic use, Multiple Sclerosis/genetics/*physiopathology, NAV1.8 Voltage-Gated Sodium Channel, Purkinje Cells/pathology/physiology, Sodium Channel Blockers/therapeutic use, Sodium Channels/biosynthesis/genetics/metabolism",
author = "Shields, {Shannon D} and Xiaoyang Cheng and Andreas Gasser and Saab, {Carl Y} and Lynda Tyrrell and Eastman, {Emmanuella M} and Masashi Iwata and Zwinger, {Pamela J} and Black, {Joel A} and Dib-Hajj, {Sulayman D} and Waxman, {Stephen G}",
year = "2012",
language = "English",
volume = "71",
pages = "186--194",
journal = "ANN NEUROL",
issn = "0364-5134",
publisher = "John Wiley and Sons Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis.

AU - Shields, Shannon D

AU - Cheng, Xiaoyang

AU - Gasser, Andreas

AU - Saab, Carl Y

AU - Tyrrell, Lynda

AU - Eastman, Emmanuella M

AU - Iwata, Masashi

AU - Zwinger, Pamela J

AU - Black, Joel A

AU - Dib-Hajj, Sulayman D

AU - Waxman, Stephen G

PY - 2012

Y1 - 2012

N2 - 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.

AB - 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.

KW - Animals

KW - Disease Models, Animal

KW - Mice

KW - Mice, Transgenic

KW - Up-Regulation/genetics

KW - Aniline Compounds/therapeutic use

KW - Cerebellar Diseases/genetics/physiopathology

KW - Cerebellum/cytology/metabolism/pathology

KW - Channelopathies/genetics/physiopathology

KW - Encephalomyelitis, Autoimmune, Experimental/drug therapy/physiopathology

KW - Furans/therapeutic use

KW - Multiple Sclerosis/genetics/physiopathology

KW - NAV1.8 Voltage-Gated Sodium Channel

KW - Purkinje Cells/pathology/physiology

KW - Sodium Channel Blockers/therapeutic use

KW - Sodium Channels/biosynthesis/genetics/metabolism

KW - Animals

KW - Disease Models, Animal

KW - Mice

KW - Mice, Transgenic

KW - Up-Regulation/genetics

KW - Aniline Compounds/therapeutic use

KW - Cerebellar Diseases/genetics/physiopathology

KW - Cerebellum/cytology/metabolism/pathology

KW - Channelopathies/genetics/physiopathology

KW - Encephalomyelitis, Autoimmune, Experimental/drug therapy/physiopathology

KW - Furans/therapeutic use

KW - Multiple Sclerosis/genetics/physiopathology

KW - NAV1.8 Voltage-Gated Sodium Channel

KW - Purkinje Cells/pathology/physiology

KW - Sodium Channel Blockers/therapeutic use

KW - Sodium Channels/biosynthesis/genetics/metabolism

M3 - SCORING: Journal article

VL - 71

SP - 186

EP - 194

JO - ANN NEUROL

JF - ANN NEUROL

SN - 0364-5134

IS - 2

M1 - 2

ER -