Deletion mutation of sodium channel NaV1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability-Reference-Cited by-同舟云学术

Deletion mutation of sodium channel NaV1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability

Published:2011-06-24 Issue:7 Volume:134 Page:1972-1986
ISSN:0006-8950
Container-title:Brain
language:en
Short-container-title:Brain

Author:

Cheng X.,Dib-Hajj S. D.,Tyrrell L.,te Morsche R. H.,Drenth J. P. H.,Waxman S. G.

Publisher

Oxford University Press (OUP)

Subject

Clinical Neurology

Link

http://academic.oup.com/brain/article-pdf/134/7/1972/17869558/awr143.pdf

Reference34 articles.

1. Antinociceptive efficacy of lacosamide in a rat model for painful diabetic neuropathy

2. Lacosamide: A Review of Preclinical Properties

3. International Union of Pharmacology. XLVII. Nomenclature and Structure-Function Relationships of Voltage-Gated Sodium Channels

4. Mutation I136V Alters Electrophysiological Properties of the NaV1.7 Channel in a Family with Onset of Erythromelalgia in the Second Decade

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