Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/9658
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Type: Journal article
Title: Tomacula in MAG-deficient mice
Author: Cai, Z.
Sutton-Smith, P.
Swift, J.
Cash, K.
Finnie, J.
Turnley, A.
Thompson, P.
Blumbergs, P.
Citation: Journal of the Peripheral Nervous System, 2002; 7(3):181-189
Publisher: Blackwell Science Inc.
Issue Date: 2002
ISSN: 1085-9489
1529-8027
Statement of
Responsibility: 
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
RMID: 0020020977
DOI: 10.1046/j.1529-8027.2002.02023.x
Appears in Collections:Medicine publications

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