Figure 2.

TH signalling regulates cell fate decision within the SVZ niche of the adult mouse. T₃ drives NSC commitment preferentially towards a neuronal fate. T₃, through its nuclear receptor TRα1, downregulates many target genes, thus promoting de novo generation of neuroblasts. In contrast, determination of glial cell fate depends on a T₃‐free window. SVZ‐OPCs are protected from the effects of T₃ by (i) the expression of DIO3 and (ii) the absence of TRα1. Later, T₃ is necessary to induce differentiation and maturation of oligodendrocytes capable to functionally repair a myelin lesion in the corpus callosum. Compared to SVZ‐OPCs (complete remyelination), resident parenchymal OPCs (thin, insufficient remyelination) are less efficient for functional brain repair