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Disturbed oligodendrocyte development and recovery from hypomyelination in a c‐myc transgenic mouse mutant
Author(s) -
Orian Jacqueline M.,
Ahern Alan J.,
Ayers Margaret M.,
Levine Joel M.,
Tapp Luke D.,
Reynolds Richard
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.1196
Subject(s) - oligodendrocyte , myelin , mutant , transgene , biology , phenotype , genetically modified mouse , myelin basic protein , microbiology and biotechnology , stimulation , neuroscience , longevity , white matter , wild type , genetics , central nervous system , gene , medicine , radiology , magnetic resonance imaging
The complexity of interactions underlying the elaboration of myelin has been extensively demonstrated. We provide evidence that signals promoting myelination are not confined to the normal developmental time window for myelination and persist well into adult life. The 2‐50 mutant, described previously, carries a c‐myc transgene regulated by a myelin basic protein promoter. This mutant is characterised by severe hypomyelination and abnormal oligodendrocytes in early life, followed by loss of the phenotype and normal longevity. We show that c‐myc expression in early oligodendrocyte development results in a substantial reduction of cells of this lineage. However, apparent complete recovery, associated with loss of c‐myc expression, axonal survival, and gradual myelin accumulation, is observed by 4 months of age. Thus, stimulation of myelination continues during adult life until normal myelin levels are established. We propose that this mutant may contribute to the characterisation of oligodendrocyte responses to myelinating signals. J. Neurosci. Res. 66:46–58, 2001. © 2001 Wiley‐Liss, Inc.