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.

The Journal of Pain
|July 31, 2023
PubMed

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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