Gonadal hormones inhibit the induction of metamorphosis by thyroid hormones in Xenopus laevis tadpoles in vivo, but not in vitro

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Although the major hormones controlling amphibian metamorphosis are those of the thyroid, other hormones, notably prolactin and the adrenal steroids, modulate the effects of thyroid hormones (TH). Some authors report that the gonadal steroids stimulate the metamorphic actions of TH whereas others report inhibition. The aims of the present study were to determine the effects of gonadal steroids on TH-induced metamorphosis in Xenopus laevis and to determine the site of action of these steroids. In all cases, hormones were added to the water in which the tadpoles were swimming. The gonadal steroids, testosterone and 17β-estradiol, inhibited triiodothyronine (T 3-induced metamorphosis in living, premetamorphic tadpoles of X. laevis. Both steroids, at 3.4 μ M, prevented the reduction in body weight and the shrinkage of head and alimentary canal brough about by 1 n M T 3. In contrast, 3.4 μ M corticosterone stimulated T 3-induced metamorphosis. Addition of 100 n M T 3 to the medium induced a large reduction in size of X. laevis tails cultured in vitro. The antagonistic effects of testosterone were not reproduced in such cultures, whereas the synergistic action of corticosterone was maintained. Testosterone had no effect upon the specific binding of T 3 to X. laevis tail tissue, whereas corticosterone increased such binding. These findings indicate that, while corticosterone stimulates the metamorphic actions of T 3 by acting directly in the peripheral tissues, the gonadal steroids, particularly testosterone, inhibit T 3 by acting at a more central site. Prolactin is known to antagonize the metamorphic actions of T 3 and one such central action could be the stimulation of prolactin synthesis. However, testosterone inhibited the prometamorphic actions of bromocriptine, which stimulates metamorphosis by inhibiting production of prolactin. Thus the central action of testoserone is unlikely to be a stimulation of prolactin production.