Cited by 159Pain Mechanisms and TreatmentsMultiple Sclerosis Research StudiesPain Management and Treatment

Neuropathic pain behaviours in a chronic-relapsing model of experimental autoimmune encephalomyelitis (EAE)

Olechowski, Camille J., Truong, Janet J., Kerr, Bradley J.·2009·Pain

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). While the primary symptoms of MS are losses of sensory and motor functions, it is now recognized that chronic pain is also a major concern affecting between 50% and 80% of MS patients. To date, however, few studies have examined the underlying mechanisms of chronic pain in MS or in the animal model, experimental autoimmune encephalomyelitis (EAE), which shares many features of MS pathology. We, therefore, set out to characterize the changes in pain sensitivity that arises in a chronic-relapsing model of EAE. We show here that female C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein (MOG(35-55)) develop a robust allodynia to both cold and tactile stimuli. Allodynia emerges early in the disease process, often before any signs of neurological deficit and is independent of the overall symptom severity in these mice. "Classical" cellular substrates for neuropathic pain and allodynia such as altered expression of sensory neuropeptides in the dorsal horn of the spinal do not appear to underlie these changes in sensory function. There is, however, a significant influx of CD3+ T cells and increased astrocyte and microglia/macrophage reactivity in the superficial dorsal horn of mice with MOG(35-55) EAE. This suggests that inflammation and reactive gliosis may be key mediators of allodynia in MOG(35-55) EAE similar to peripheral nerve and spinal cord injury models. Taken together, our results show that the MOG(35-55) EAE model is a useful tool to study neuropathic pain in MS.

Integrity signals

Registry

Crossref · 10.1016/j.pain.2008.11.002

Cites

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  • Autoimmune encephalomyelitis has been postulated to underlie the development of neuropathic pain in multiple sclerosis.

    “autoimmune encephalomyelitis has been postulated to underlie the development of neuropathic pain in MS.”
  • Cold and mechanical allodynia, but not thermal hyperalgesia, have been reported in a model of autoimmune encephalomyelitis in which mice were immunized with myelin oligodendrocyte glycoprotein (MOG(35-55)).

    “Cold and mechanical allodynia, but not thermal hyperalgesia, have been reported in a model of autoimmune encephalomyelitis in which mice were immunized with myelin oligodendrocyte glycoprotein (MOG(35-55))128”

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Authors
Olechowski, C. J., Truong, J. J., & Kerr, B. J.
Affiliations
University of Alberta (CA)
Corresponding author
Kerr, Bradley J.
Venue
Pain
Published
2009-01
Volume
141
Issue
1
Pages
156-164
ISSN
0304-3959 (ISSN-L)
OpenAlex
W2021568221
Cited by
159
References
42
Citations by year
2026: 1 · 2025: 1 · 2024: 5 · 2023: 5 · 2022: 7 · 2021: 15 · 2020: 12 · 2019: 13 · 2018: 8 · 2017: 9 · 2016: 10 · 2015: 11 · 2014: 11 · 2013: 22 · 2012: 8
FWCI
4.74
Type
journal article
Language
en
Open access
closed
Locations
  • Pain (publishedVersion)
  • PubMed (publishedVersion)
Funders
Multiple Sclerosis Society
Topics
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
Keywords
neuropathic pain, multiple sclerosis, experimental autoimmune encephalomyelitis, allodynia, myelin oligodendrocyte glycoprotein, MOG35-55, chronic pain, dorsal horn, CD3+ T cells, astrocyte activation, reactive gliosis, sensory neuropeptides, C57BL/6 mice
MeSH terms
Analysis of Variance, Animals, Antigens, Differentiation, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, Female, Gliosis, Glycoproteins, Hyperalgesia, Mice, Inbred C57BL, Motor Activity, Neuralgia, Peptide Fragments, Reaction Time, Spinal Cord, Antigens, CD, Calcitonin Gene-Related Peptide, Pain Threshold, Disease Progression, Mice, Myelin-Oligodendrocyte Glycoprotein

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