Mice deficient for the glycoprotein show subtle abnormalities in myelin

Dirk Montag, Karl Peter Giese, Udo Bartsch, Rudolf Martini, Yolande Lang, Horst Blüthmann, Jeevajothie Karthigasan, Daniel A. Kirschner, Eva S. Wintergerst, Klaus Armin Nave, Jürgen Zielasek, Klaus V. Toyka, Hans Peter Lipp, Melitta Schachner

Research output: Contribution to journalArticlepeer-review

314 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)229-246
Number of pages18
JournalNeuron
Volume13
Issue number1
DOIs
StatePublished - Jul 1994
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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