Absence of the myelin-associated glycoprotein (MAG) and the neural cell adhesion molecule (N-CAM) interferes with the maintenance,but not with the formation of peripheral myelin |
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Authors: | Stefano Carenini Dirk Montag Harold Cremer Melitta Schachner Rudolf Martini |
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Institution: | Department of Neurobiology, Swiss Federal Institute of Technology, H?nggerberg, CH-8093 Zürich, Switzerland, CH LGPD, IBDM, CNRS-INSERM, Campus de Luminy, cas 907, F-13288 Marseille cedex 9, France, FR
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Abstract: | We have previously shown that mice deficient in the gene for the myelin-associated glycoprotein (MAG) develop normal myelin
in the peripheral nerves, but show axon and myelin degeneration at eight months of age, suggesting that MAG is involved in
the maintenance of axon-Schwann cell integrity. The search for molecules that might replace MAG during myelination revealed
an overexpression of the neural cell adhesion molecule (N-CAM) at those aspects where MAG is detectable in wild type mice.
To test whether N-CAM might compensate for MAG during myelination in MAG-deficient mice, double mutants deficient in both
MAG and N-CAM (MAG−/N-CAM−mice) were generated by cross-breeding the single mutants. Whereas alterations of myelin development were not detectable in
either of the single or double mutants, degeneration of myelin and axons occurred approximately 4 weeks earlier in MAG−/N-CAM−than in MAG−mutants. Furthermore, at 8 weeks of age, single fiber preparation and electron microscopy revealed that the number of profiles
indicative of degeneration was substantially increased in MAG−/N-CAM−mutants when compared to MAG−mice. These data suggest that in MAG-deficient mice N-CAM does not compensate for MAG in myelin formation but partially substitutes
for it in the maintenance of axon-myelin integrity.
Received: 20 May 1996 / Accepted: 19 July 1996 |
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Keywords: | : Schwann cell Peripheral nerve Adhesion molecules Knock-out Redundancy Mouse (N-CAM MAG ) |
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