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Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
Published on: April 15, 2014
A Novel Sensory Wave (P25) in Myelin Oligodendrocyte Glycoprotein-induced Experimental Autoimmune Encephalomyelitis
Yoav Shulman1, Lena Finkelstein1, Yakir Levi1
1Neurology Division, MD Biosciences Innovalora, Ltd, Rehovot, Israel.
Abstract:
Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is a murine model for multiple sclerosis. This model is characterized by chronic and progressive demyelination, leading to impairment of motor function and paralysis. While the outcomes of the disease, including impaired motor function and immunological changes, are well-characterized, little is known about the impact of EAE on the electrophysiology of the motor and sensory systems. In this study, we assessed evoked potentials as a quantitative marker for in vivo monitoring of nervous system damage. Motor-evoked potentials (MEPs) and sensory-evoked potentials (SEPs) were first standardized in naïve C57BL mice and studied thoroughly in EAE mice. The duration of MEPs and the number of connotative potentials increased significantly alongside an increase in temporal SEP amplitudes. Moreover, a new SEP wave was identified in naïve animals, which significantly increased in MOG-induced EAE animals with no or mild symptoms (clinical score 0-2, 0-5 scale). This wave occurred ∼25 milliseconds poststimulation, thus named p25. P25 was correlated with increased vocalization and was also reduced in amplitude following treatment with morphine. As the EAE score progressed (clinical score 3-4, 0-5 scale), the amplitude of MEPs and SEPs decreased drastically. Our results demonstrate that desynchronized neural motor activity, along with hypersensitivity in the early stages of EAE, leads to a complete loss of motor and sensory functions in the late stages of the disease. The findings also suggest an increase in p25 amplitude before motor deficits appear, indicating SEP as a predictive marker for disease progression. PERSPECTIVE: This article assesses p25, a new sensory electrophysiology wave that correlates with pain-related behavior in MOG-induced EAE mice and appears prior to the clinical symptoms. Motor electrophysiology correlates with traditional motor behavior scoring and histology.
Insights
Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in mice shows altered electrophysiology. A new sensory evoked potential wave (p25) predicts disease progression before motor symptoms appear.
Area of Science:
- Neuroscience
- Immunology
- Electrophysiology
Background:
- Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is a mouse model for multiple sclerosis, characterized by demyelination and motor impairment.
- While disease outcomes are known, the electrophysiological impact on motor and sensory systems in EAE remains poorly understood.
Purpose of the Study:
- To investigate the in vivo electrophysiological changes in motor and sensory systems during MOG-induced EAE.
- To identify potential electrophysiological markers for early disease detection and progression.
Main Methods:
- Standardized motor-evoked potentials (MEPs) and sensory-evoked potentials (SEPs) in naïve C57BL mice.
- Assessed MEPs and SEPs in MOG-induced EAE mice at different disease stages.
- Identified and characterized a novel SEP wave, termed p25.
Main Results:
- MEP duration and SEP temporal amplitudes increased in early EAE.
- A new SEP wave (p25) emerged and increased in amplitude in early EAE, correlating with vocalization and morphine response.
- MEP and SEP amplitudes significantly decreased in late-stage EAE, correlating with severe motor deficits.
Conclusions:
- Electrophysiological changes, including the novel p25 wave, reflect disease progression in MOG-induced EAE.
- The p25 wave serves as a potential predictive marker for EAE development and progression.
- Electrophysiology provides quantitative insights into nervous system damage and functional loss in EAE.
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