• Marijke Stevens, Silke Timmermans, Astrid Bottelbergs, Jerome J A Hendriks, Bert Brône, Myriam Baes, and Jan Tytgat.
• Laboratory of Toxicology, Department of Pharmaceutical Sciences, KU Leuven, Campus Gasthuisberg O&N2, Herestraat 49 Box 922, B-3000 Leuven, Belgium.
• J. Neuroimmunol. 2013 Aug 15; 261 (1-2): 21-8.

AbstractVoltage-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.Copyright © 2013 Elsevier B.V. All rights reserved.

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