Mice deficient for the myelin-associated glycoprotein show subtle abnormalities in myelin
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Mice deficient for the myelin-associated glycoprotein show subtle abnormalities in myelin. / Montag, D; Giese, K P; Bartsch, U; Martini, R; Lang, Y; Blüthmann, H; Karthigasan, J; Kirschner, D A; Wintergerst, E S; Nave, K A.
In: NEURON, Vol. 13, No. 1, 07.1994, p. 229-46.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Mice deficient for the myelin-associated glycoprotein show subtle abnormalities in myelin
AU - Montag, D
AU - Giese, K P
AU - Bartsch, U
AU - Martini, R
AU - Lang, Y
AU - Blüthmann, H
AU - Karthigasan, J
AU - Kirschner, D A
AU - Wintergerst, E S
AU - Nave, K A
PY - 1994/7
Y1 - 1994/7
N2 - 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.
AB - 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.
KW - Animals
KW - Base Sequence
KW - Behavior, Animal
KW - Brain
KW - Cell Adhesion Molecules, Neuronal
KW - DNA
KW - Female
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Mice, Transgenic
KW - Microscopy, Electron
KW - Molecular Sequence Data
KW - Mutation
KW - Myelin Proteins
KW - Myelin Sheath
KW - Myelin-Associated Glycoprotein
KW - Oligodendroglia
KW - Optic Nerve
KW - Peripheral Nerves
KW - RNA, Messenger
KW - Restriction Mapping
KW - Schwann Cells
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
KW - Research Support, U.S. Gov't, P.H.S.
M3 - SCORING: Journal article
C2 - 7519026
VL - 13
SP - 229
EP - 246
JO - NEURON
JF - NEURON
SN - 0896-6273
IS - 1
ER -