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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 oligodendroglial 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.
Pubmed ID: 18760695 RIS Download
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Data analysis software for neurophysiology with a multitude of features, including: * Import of native data files created by many popular data acquisition systems * All standard histogram and raster analyses * Shift predictors in crosscorrelograms and color markers in perievent rasters * Joint PSTH, burst analysis and many more analyses of timestamped data * Spectral analysis of spike and continuous data * 3D data view and animation * Fully customizable WYSIWYG graphics * Custom analysis and batch mode processing with internal scripting language * Direct data link to Matlab and Excel * Statistical tests via direct link to R-project
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