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Updated: Oct 14, 2026

Simple and Efficient Production and Purification of Mouse Myelin Oligodendrocyte Glycoprotein for Experimental Autoimmune Encephalomyelitis Studies
10:47

Simple and Efficient Production and Purification of Mouse Myelin Oligodendrocyte Glycoprotein for Experimental Autoimmune Encephalomyelitis Studies

Published on: October 27, 2016

Oligodendrocytes and their myelin-plasma membrane connections in JHM mouse hepatitis virus encephalomyelitis

H C Powell, P W Lampert

    Laboratory Investigation; a Journal of Technical Methods and Pathology
    |October 1, 1975
    PubMed

    Insights

    Mouse hepatitis virus infects oligodendrocytes, causing demyelinating encephalomyelitis in mice. Altered myelin-plasma membrane connections in infected cells may explain recurrent demyelination post-infection.

    Area of Science:

    • Neurovirology
    • Cell Biology
    • Pathogenesis of Demyelinating Diseases

    Background:

    • Mouse hepatitis virus (JHM strain) causes demyelinating encephalomyelitis in mice.
    • Demyelination involves myelin sheath stripping by macrophages following oligodendrocyte degeneration.

    Purpose of the Study:

    • To investigate the ultrastructural changes in oligodendrocytes during JHMV infection.
    • To elucidate the role of oligodendrocyte pathology in the pathogenesis of demyelination.

    Main Methods:

    • Electron microscopy was used to examine infected mouse brains.
    • Ultrastructural analysis focused on oligodendrocytes and their interaction with myelin.

    Main Results:

    • JHMV replicates within oligodendrocytes, leading to their hypertrophy and degeneration.
    • Hypertrophic oligodendrocytes exhibit abundant organelles and unique plasma membrane connections to myelin.
    • Degenerating cells show vacuolar and hydropic changes.

    Conclusions:

    • Infected oligodendrocytes undergo significant ultrastructural alterations before degeneration.
    • Altered myelin-plasma membrane connections in infected oligodendrocytes are implicated in demyelination.
    • These findings provide insights into the pathogenesis of post-infectious demyelination.

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