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|Title:||Tomacula in MAG-deficient mice|
|Citation:||Journal of the Peripheral Nervous System, 2002; 7(3):181-189|
|Publisher:||Blackwell Science Inc.|
|Zhao Cai, Peter Sutton-Smith, Jeffrey Swift, Kathy Cash, John Finnie, A Turnley, Philip D Thompson, Peter C Blumbergs|
|Abstract:||The pathogenesis of tomacula in mice with a null mutation of the myelin-associated glycoprotein (MAG) gene is not well understood. This study, using a novel teased nerve fiber technique, demonstrates that tomacula in MAG-deficient mice are formed by redundant myelin infoldings and outfoldings in the paranodal regions as early as 4 weeks after birth and increase in size and frequency with age. Although tomacula show degenerative changes with increasing age, there was no significant evidence of demyelination/remyelination. Longitudinal sections of normal teased nerve fibers show early redundant myelin foldings in externally normal paranodal regions. These data and the absence of internodal tomacula support a role for MAG in the maintenance of myelin at the paranodal regions.|
|Keywords:||Myelin Sheath; Nerve Fibers; Animals; Mice, Knockout; Mice; Nerve Degeneration; Myelin-Associated Glycoprotein; Hereditary Sensory and Motor Neuropathy|
|Description:||The definitive version is available at www.blackwell-synergy.com|
|Appears in Collections:||Medicine publications|
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