Mechanical hypernociception in experimental autoimmune encephalomyelitis

Arq Neuropsiquiatr. 2009 Mar;67(1):78-81. doi: 10.1590/s0004-282x2009000100019.

Abstract

Background: Pain is an important clinical manifestation in multiple sclerosis (MS) patients, though it has been neglected in clinical and experimental researches.

Objective: To investigate the nociceptive response in MOG35-55 experimental autoimmune encephalomyelitis (EAE)-induced mice.

Method: EAE was induced in 8 to 10 week old C57BL/6 female mice with an emulsion of MOG35-55, Complete Freund Adjuvant, Mycobacterium tuberculosis H37 RA and pertussis toxin. Nociception was evaluated by the von Frey filaments method. A clinical scale ranging from 0 to 15 was used to assess motor impairment.

Results: Clinical evidence of disease started at day 10 and peaked at day 14 after immunization. Thereafter, there was no worsening of symptoms until day 26. The EAE-induced mice presented reduced pressure threshold at days 7th and 10th after immunization and before the onset of clinical motor signs.

Conclusion: The hypernociception found validates MOG35-55 EAE as a model for the study of pain in multiple sclerosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Encephalomyelitis, Autoimmune, Experimental / chemically induced
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Female
  • Glycoproteins
  • Mice
  • Mice, Inbred C57BL
  • Multiple Sclerosis / physiopathology*
  • Myelin Proteins
  • Myelin-Associated Glycoprotein
  • Myelin-Oligodendrocyte Glycoprotein
  • Nerve Tissue Proteins
  • Nociceptors / physiology*
  • Peptide Fragments

Substances

  • Glycoproteins
  • Mog protein, mouse
  • Myelin Proteins
  • Myelin-Associated Glycoprotein
  • Myelin-Oligodendrocyte Glycoprotein
  • Nerve Tissue Proteins
  • Peptide Fragments
  • myelin oligodendrocyte glycoprotein (35-55)