Referenced in: none

Automatically associated channels: Nav1.2 , Nav1.4 , Nav1.6

Title: Block of a subset of sodium channels exacerbates experimental autoimmune encephalomyelitis.

Authors: Marijke Stevens, Silke Timmermans, Astrid Bottelbergs, Jerome J A Hendriks, Bert Brône, Myriam Baes, Jan Tytgat

Journal, date & volume: J. Neuroimmunol., 2013 Aug 15 , 261, 21-8

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/23735284

Abstract
Voltage-gated sodium channels (Navs) are involved in several aspects of the pathogenesis of multiple sclerosis (MS). Within acute MS plaques, they are expressed along demyelinated axons. Studies in experimental autoimmune encephalomyelitis (EAE) demonstrated a neuroprotective effect of non-specific Nav blockers. Further, block of specific Navs involved in MS is suggested to have an advantage over non-specific blockers. We investigated the effects of the synthetic Midi peptide in EAE, as it potently and specifically blocks Nav1.2, Nav1.4 and Nav1.6. Administration of this Midi peptide worsens the clinical disease pattern and Nav1.2 and Nav1.6 expression levels were elevated in brain but not in spinal cord of Midi-treated mice, implicating that Navs play a complex role in the pathogenesis of EAE.