Neuropathic pain behaviours in a chronic-relapsing model of experimental autoimmune encephalomyelitis (EAE)
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.
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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.”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [128]
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”
From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [128]
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Austin, P. J., & Moalem-Taylor, G. (2010) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2010.08.013 · Cited by 607 · see citing works
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- Authors
- Olechowski, C. J., Truong, J. J., & Kerr, B. J.
- Affiliations
- University of Alberta (CA)
- Corresponding author
- Kerr, Bradley J.
- ORCID
- 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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