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Related Experiment Videos

Tomacula in MAG-deficient mice.

Zhao Cai1, Peter Sutton-Smith, Jeffrey Swift

  • 1Department of Neurology, Royal Adelaide Hospital, South Australia.

Journal of the Peripheral Nervous System : JPNS
|October 9, 2002
PubMed
Summary

Myelin-associated glycoprotein (MAG) deficiency causes redundant myelin folds in mouse nerve paranodes, forming tomacula. These structures increase with age, suggesting MAG is crucial for maintaining myelin integrity at paranodal regions.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Tomacula formation in myelin-associated glycoprotein (MAG) deficient mice is not well understood.
  • MAG plays a role in myelin maintenance, but its specific function in paranodal regions requires further investigation.

Purpose of the Study:

  • To investigate the pathogenesis of tomacula in MAG-deficient mice.
  • To elucidate the role of MAG in maintaining myelin structure at the paranodal regions.

Main Methods:

  • Utilized a novel teased nerve fiber technique.
  • Examined longitudinal sections of nerve fibers from MAG-deficient and normal mice at various ages.

Main Results:

  • Tomacula, formed by redundant myelin infoldings/outfoldings, were observed in paranodal regions of MAG-deficient mice as early as 4 weeks after birth.

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  • The size and frequency of tomacula increased with age in MAG-deficient mice.
  • No significant demyelination or remyelination was observed, despite age-related degenerative changes in tomacula.

    • Conclusions:

    • MAG deficiency leads to the formation of tomacula due to aberrant myelin folding in paranodal regions.
    • MAG is essential for the structural integrity of myelin at the paranodal regions.
    • The absence of internodal tomacula further supports MAG's specific role in paranodal myelin maintenance.