4-Aminopyridine ameliorates relapsing remitting experimental autoimmune encephalomyelitis in SJL/J mice

J Neuroimmunol. 2018 Oct 15:323:131-135. doi: 10.1016/j.jneuroim.2018.08.007. Epub 2018 Aug 18.

Abstract

We evaluated the effects of a non-specific potassium channel blocker, 4-aminopyridine (4-AP), on chronic experimental autoimmune encephalomyelitis (chEAE) and relapsing remitting EAE (rrEAE) in mice. 4-AP did not affect chEAE, but ameliorated rrEAE, particularly in the relapsing phase. Disease amelioration was confirmed pathologically, and glial fibrillary acidic protein expression was observed to be downregulated in 4-AP-treated mice. In the recall response, a T-cell proliferative response was not inhibited; however, Th1/Th17 polarization was attenuated. 4-AP is currently accepted as an anti-symptomatic drug only in the chronic phase of multiple sclerosis (MS); however, its use in the active phase of MS should be considered.

Keywords: 4-aminopyridine; Experimental autoimmune encephalomyelitis; Potassium channel.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 4-Aminopyridine / pharmacology
  • 4-Aminopyridine / therapeutic use*
  • Amino Acid Sequence
  • Animals
  • Encephalomyelitis, Autoimmune, Experimental / diagnosis*
  • Encephalomyelitis, Autoimmune, Experimental / drug therapy*
  • Encephalomyelitis, Autoimmune, Experimental / genetics
  • Female
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Potassium Channel Blockers / pharmacology
  • Potassium Channel Blockers / therapeutic use*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / physiology

Substances

  • Potassium Channel Blockers
  • 4-Aminopyridine