Thyroid hormone (TH) is essential for vertebrate brain development. Most 
research on TH and neuronal development focuses on late development, mainly the 
perinatal period in mammals. However, in human infants neuromotor development 
correlates best with maternal TH levels in the first trimester of pregnancy, 
suggesting that TH signaling could affect early brain development. Studying TH 
signaling in early embryogenesis in mammals is experimentally challenging. In 
contrast, free-living embryos, such as Xenopus laevis, permit physiological 
experimentation independent of maternal factors. We detailed key elements of TH 
signaling: ligands, receptors (TR), and deiodinases during early X. laevis 
development, before embryonic thyroid gland formation. Dynamic profiles for all 
components were found. Between developmental stages 37 and 41 (~48 h after 
hatching, coincident with a phase of continuing neurogenesis) significant 
increases in T(3) levels as well as in mRNA encoding deiodinases and TR 
occurred. Exposure of embryos at this developmental stage for 24 h to either a 
TH antagonist, NH-3, or to tetrabromobisphenol A, a flame retardant and known TH 
disruptor, differentially modulated the expression of a number of TH target 
genes implicated in neural stem cell function or neural differentiation. 
Moreover, 24-h exposure to either NH-3 or tetrabromobisphenol A diminished cell 
proliferation in the brain. Thus, these data show first, that TH signaling 
exerts regulatory roles in early X. laevis neurogenesis and second, that this 
period represents a potential window for endocrine disruption.