Hyperalgesia in an animal model of multiple sclerosis

Sue Aicher, Marc B. Silverman, Clayton W. Winkler, Bruce F. Bebo

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

Many individuals with multiple sclerosis (MS) experience clinically significant pain, yet the underlying neural mechanisms for MS pain are not understood. Experimental autoimmune encephalomyelitis (EAE) is a well-studied disease in rodents that mimics many clinical and pathological features of MS, including central nervous system inflammation and demyelination. To determine whether EAE is an appropriate model for MS-related pain, nociceptive responses in both male and female SJL mice were measured before and after immunization with myelin proteolipid protein peptide 139-151 (PLP139-151) in complete Freund's adjuvant to induce 'active' EAE. To determine if changes in nociception were due to direct effects of encephalitogenic T cells, nociceptive responses in female SJL mice were measured following the transfer of activated, PLP139-151 specific T cells to induce 'passive' EAE. Both forepaw and tail withdrawal latencies to a radiant heat stimulus were measured. In both active and passive EAE, there was an initial increase in tail withdrawal latency (hypoalgesia) that peaked several days prior to the peak in motor deficits during the acute disease phase. During the chronic disease phase, tail withdrawal latencies decreased and were significantly faster than control latencies for up to 38 days post-immunization. This hyperalgesia was seen in both sexes and in both active and passive EAE models. Forepaw withdrawal latencies remained within 1-2 s of baseline latencies for the entire testing period, indicating that the hypoalgesia and hyperalgesia were most pronounced in clinically affected body regions. These results suggest that both active and passive EAE are useful models of MS-related pain.

Original languageEnglish (US)
Pages (from-to)560-570
Number of pages11
JournalPain
Volume110
Issue number3
DOIs
StatePublished - Aug 2004

Fingerprint

Autoimmune Experimental Encephalomyelitis
Hyperalgesia
Multiple Sclerosis
Animal Models
Tail
Pain
Immunization
Rodent Diseases
Nociceptive Pain
T-Lymphocytes
Body Regions
Peptides
Nociception
Freund's Adjuvant
Demyelinating Diseases
Acute Disease
Chronic Disease
Central Nervous System
Hot Temperature
Inflammation

Keywords

  • Central nervous system
  • Hyperalgesia
  • Multiple sclerosis

ASJC Scopus subject areas

  • Clinical Neurology
  • Psychiatry and Mental health
  • Neurology
  • Neuroscience(all)
  • Pharmacology
  • Clinical Psychology

Cite this

Aicher, S., Silverman, M. B., Winkler, C. W., & Bebo, B. F. (2004). Hyperalgesia in an animal model of multiple sclerosis. Pain, 110(3), 560-570. https://doi.org/10.1016/j.pain.2004.03.025

Hyperalgesia in an animal model of multiple sclerosis. / Aicher, Sue; Silverman, Marc B.; Winkler, Clayton W.; Bebo, Bruce F.

In: Pain, Vol. 110, No. 3, 08.2004, p. 560-570.

Research output: Contribution to journalArticle

Aicher, S, Silverman, MB, Winkler, CW & Bebo, BF 2004, 'Hyperalgesia in an animal model of multiple sclerosis', Pain, vol. 110, no. 3, pp. 560-570. https://doi.org/10.1016/j.pain.2004.03.025
Aicher, Sue ; Silverman, Marc B. ; Winkler, Clayton W. ; Bebo, Bruce F. / Hyperalgesia in an animal model of multiple sclerosis. In: Pain. 2004 ; Vol. 110, No. 3. pp. 560-570.
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