SYNOPSIS. The climactic stages of amphibian metamorphosis constitute a period characterized by radical morphological changes that are driven primarily by the thyroidal hormones. Radioimmunoassays show that levels of thyroid hormones (TH) rise to a peak during metamorphic climax. Accompanying peaks are reported for ACTH, adrenal corticoids (AC), insulin (I) and prolacdn (PRL). AC enhance the metamorphic action of TH by increasing their binding to nuclei of target cells. TH, in turn, act to raise levels of AC by stimulating the differentiation of the median eminence thus facilitating the flow of a CRF from the hypothalamus to the adenohypophysis, by synergizing with ACTH and bystimulation of the interrenals through some other route. During the metamorphic period, at least as far as climax, PRL antagonizes TH, perhaps at the thyroidal level and certainly at the level of target cells. PRL may antagonize by inhibiting induction of hydrolytic enzymes by TH, by alteration of hydromineral responses or by altering levels of binding of TH to receptors. The antagonistic action of PRL is mimicked by cAMP. A surge of PRL that is released into the plasma during metamorphic climax seemingly produces no antagonistic effect on thyroidal actions.