The subventricular zone (SVZ) neural stem cell niche contains mixed populations 
of stem cells, transit-amplifying cells, and migrating neuroblasts. Deciphering 
how endogenous signals, such as hormones, affect the balance between these cell 
types is essential for understanding the physiology of niche plasticity and 
homeostasis. We show that Thyroid Hormone (T(3)) and its receptor, TRα1, are 
directly involved in maintaining this balance. TRα1 is expressed in amplifying 
and migrating cells. In vivo gain- and loss-of-function experiments demonstrate 
first, that T(3)/TRα1 directly repress Sox2 expression, and second, that TRα1 
overexpression in the niche favors the appearance of DCX+ migrating neuroblasts. 
Lack of TRα increases numbers of SOX2+ cells in the SVZ. Hypothyroidism 
increases proportions of cells in interphase. Thus, in the adult SVZ, T(3)/TRα1 
together favor neural stem cell commitment and progression toward a migrating 
neuroblast phenotype; this transition correlates with T(3)/TRα1-dependent 
transcriptional repression of Sox2.