Format

Send to

Choose Destination
Neuron. 1994 Jul;13(1):229-46.

Mice deficient for the myelin-associated glycoprotein show subtle abnormalities in myelin.

Author information

1
Department of Neurobiology, Swiss Federal Institute of Technology Hönggerberg, Zürich, Switzerland.

Abstract

Using homologous recombination in embryonic stem cells, we have generated mice with a null mutation in the gene encoding the myelin-associated glycoprotein (MAG), a recognition molecule implicated in myelin formation. MAG-deficient mice appeared normal in motor coordination and spatial learning tasks. Normal myelin structure and nerve conduction in the PNS, with N-CAM overexpression at sites normally expressing MAG, suggested compensatory mechanisms. In the CNS, the onset of myelination was delayed, and subtle morphological abnormalities were detected in that the content of oligodendrocyte cytoplasm at the inner aspect of most myelin sheaths was reduced and that some axons were surrounded by two or more myelin sheaths. These observations suggest that MAG participates in the formation of the periaxonal cytoplasmic collar of oligodendrocytes and in the recognition between oligodendrocyte processes and axons.

PMID:
7519026
DOI:
10.1016/0896-6273(94)90472-3
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center