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Updated: Jun 24, 2026

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis
Published on: February 23, 2024
Mechanical hypernociception in experimental autoimmune encephalomyelitis
David Henrique Rodrigues1, Daniela Sachs, Antonio Lucio Teixeira
1Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.
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.
Insights
This study shows that mice with experimental autoimmune encephalomyelitis (EAE) experience increased pain sensitivity before motor symptoms appear. This validates the MOG35-55 EAE model for studying pain in multiple sclerosis.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Pain is a significant but understudied clinical symptom in multiple sclerosis (MS).
- Understanding pain mechanisms in MS is crucial for improving patient care.
Purpose of the Study:
- To investigate nociceptive responses in mice with MOG35-55 induced experimental autoimmune encephalomyelitis (EAE).
- To establish the MOG35-55 EAE model as a viable tool for pain research in MS.
Main Methods:
- Experimental autoimmune encephalomyelitis (EAE) was induced in female C57BL/6 mice using MOG35-55 emulsion and adjuvants.
- Nociception was assessed using the von Frey filaments method.
- Motor impairment was evaluated using a clinical scale (0-15).
Main Results:
- Clinical signs of EAE emerged around day 10, peaking at day 14.
- Mice exhibited reduced pressure thresholds on days 7 and 10 post-immunization, preceding motor deficits.
- The EAE model demonstrated hypernociception prior to the onset of clinical motor impairment.
Conclusions:
- The observed hypernociception confirms the MOG35-55 EAE model's utility.
- This model is suitable for studying pain mechanisms in the context of multiple sclerosis.
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