Several environmental chemicals disrupt thyroid function, a key regulator of normal development involved in many physiological processes in fish. We studied the effects of such chemicals in vivo using transient transgenic zebrafish ( Danio rerio), expressing Green Fluorescent Protein (GFP) under the control of a TH/bZIP promoter from Xenopus laevis. Exposure to thyroid hormone (T3) at 10 −8 M increased GFP fluorescence in F0 embryos and larvae. Transient transgenic embryos were exposed to a T3 signaling agonist (TRIAC) or antagonists (NH 3 or NaClO 4), or to the endocrine disruptor Bisphenol A (BPA). When tested alone, TRIAC increased fluorescence, confirming the specificity of our model. Exposure to NH 3 or NaClO 4 decreased fluorescence, reflecting inhibition of thyroid function. When tested alone, BPA did not modify fluorescence, but when tested with T3, it significantly reduced T3-induced fluorescence, suggesting disruption of the thyroid function by BPA. The expression of genes involved in the TH axis (TR-alpha, TR-beta, TSH) and the corticoid axis (GR and MR) was followed by q-PCR after T3 or BPA exposure (24 or 48 h) and at different developmental stages (0, 1, or 5 days post-fertilization). Expression of TR-alpha, TR-beta, and TSH genes increased after 48 h T3 exposure in 1-day-old larvae. When tested alone, BPA only slightly affected gene expression. When applied with T3, BPA decreased expression of all candidate genes in 1-day-old embryos compared to the T3 treated group, in agreement with data obtained with the TH/bZIP-eGFP zebrafish model. Finally, we show that T3 exposure leads to up-regulation of MR and GR genes. This study provides a new rapid diagnostic tool for characterizing the disrupting effects of toxicants on thyroid function and suggests possible crosstalk between the TR and Corticoid Signaling system.