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Updated: May 18, 2026
Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Pain in experimental autoimmune encephalitis: a comparative study between different mouse models
Jianning Lu1, Martina Kurejova, Laura N Wirotanseng
1Pharmacology Institut, University of Heidelberg, Im Neuenheimer Feld 366, Heidelberg, D-69120, Germany.
Background:
Pain can be one of the most severe symptoms associated with multiple sclerosis (MS) and develops with varying levels and time courses. MS-related pain is difficult to treat, since very little is known about the mechanisms underlying its development. Animal models of experimental autoimmune encephalomyelitis (EAE) mimic many aspects of MS and are well-suited to study underlying pathophysiological mechanisms. Yet, to date very little is known about the sensory abnormalities in different EAE models. We therefore aimed to thoroughly characterize pain behavior of the hindpaw in SJL and C57BL/6 mice immunized with PLP139-151 peptide or MOG35-55 peptide respectively. Moreover, we studied the activity of pain-related molecules and plasticity-related genes in the spinal cord and investigated functional changes in the peripheral nerves using electrophysiology.
Methods:
We analyzed thermal and mechanical sensitivity of the hindpaw in both EAE models during the whole disease course. Qualitative and quantitative immunohistochemical analysis of pain-related molecules and plasticity-related genes was performed on spinal cord sections at different timepoints during the disease course. Moreover, we investigated functional changes in the peripheral nerves using electrophysiology.
Results:
Mice in both EAE models developed thermal hyperalgesia during the chronic phase of the disease. However, whereas SJL mice developed marked mechanical allodynia over the chronic phase of the disease, C57BL/6 mice developed only minor mechanical allodynia over the onset and peak phase of the disease. Interestingly, the magnitude of glial changes in the spinal cord was stronger in SJL mice than in C57BL/6 mice and their time course matched the temporal profile of mechanical hypersensitivity.
Conclusions:
Diverse EAE models bearing genetic, clinical and histopathological heterogeneity, show different profiles of sensory and pathological changes and thereby enable studying the mechanistic basis and the diversity of changes in pain perception that are associated with distinct types of MS.
Insights
Multiple sclerosis (MS) pain mechanisms were studied in mouse models. Different models showed varied pain profiles and spinal cord changes, aiding understanding of MS pain diversity.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Multiple sclerosis (MS) causes severe pain, but its mechanisms are poorly understood.
- Experimental autoimmune encephalomyelitis (EAE) models offer insights into MS pathophysiology.
- Sensory abnormalities in EAE models require thorough characterization.
Purpose of the Study:
- To characterize hindpaw pain behavior in two distinct EAE mouse models.
- To investigate molecular and genetic changes in the spinal cord related to pain.
- To assess functional alterations in peripheral nerves.
Main Methods:
- Assessed thermal and mechanical sensitivity in EAE mice throughout disease progression.
- Conducted immunohistochemical analysis of pain and plasticity molecules in spinal cords.
- Utilized electrophysiology to examine peripheral nerve function.
Main Results:
- Both EAE models exhibited thermal hyperalgesia in the chronic phase.
- SJL mice developed significant mechanical allodynia, unlike C57BL/6 mice.
- Glial changes in the spinal cord correlated with mechanical hypersensitivity, particularly in SJL mice.
Conclusions:
- Heterogeneous EAE models display distinct sensory and pathological changes.
- These models facilitate the study of mechanisms underlying diverse MS pain profiles.
- Understanding these differences is crucial for developing targeted MS pain therapies.
