Journal
NEURON
Volume 59, Issue 4, Pages 581-595Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2008.06.028
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Funding
- Deutsche Forschungsgemeinschaft
- National Multiple Sclerosis Society
- Hertie Institute of MS Research
- Myelin Project
- BMBF
- Deutsche Forschungsgemeinschaft [SFB 665]
- National Institutes of Health [NS32367]
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Understanding the control of myelin formation by oligodendrocytes is essential for treating demyelinating diseases. Neuregulin-1 (NRG1) type III, an EGF-like growth factor, is essential for myelination in the PNS. It is thus thought that NRG1/ErbB signaling also regulates CNS myelination, a view suggested by in vitro studies and the overexpression of dominant-negative ErbB receptors. To directly test this hypothesis, we generated a series of conditional null mutants that completely lack NRG1 beginning at different stages of neural development. Unexpectedly, these mice assemble normal amounts of myelin. In addition, double mutants lacking oligo-dendroglial ErbB3 and ErbB4 become myelinated in the absence of any stimulation by neuregulins. In contrast, a significant hypermyelination is achieved by transgenic overexpression of NRG1 type I or NRG1 type III. Thus, NRG1/ErbB signaling is markedly different between Schwann cells and oligodendrocytes that have evolved an NRG/ErbB-independent mechanism of myelination control.
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