Abstract

Metamorphosis in the Mexican axolotl was induced by daily injection of purified ovine TSH, but not by injection of large doses of iodide. Thyroxine was effective in inducing metamorphosis when injected in a dose as low as 0.5 μg per 100 g per day, suggesting that axolotl tissue is normally sensitive to thyroid hormone. It is unlikely, therefore, that neoteny in this species is attributable to tissue resistance to the action of thyroid hormone. Thyroid 131I uptakes in axolotls were of the order of 1–2% after 48 hr, and 131T-T 4 comprised only 2–4% of the total. 131I-T 4 was not detected in the circulation. After chronic administration of TSH, thyroid 131I uptakes rose greatly, 131I-T 4 comprised 15–18% of glandular 131I, and 131I-T 4 was readily detectable in the circulation. In all these respects 131I metabolism in the axolotl resembled that seen previously in hypophysectomized rats. These results support the view that failure of metamorphosis in Ambystoma mexicanum is related to a very low rate of TSH secretion by the pituitary. Chronic injection of long-acting thyroid stimulator induced none of the changes associated with metamorphosis in Mexican axolotls and bad no effect on thyroid 131I metabolism. Plasma protein patterns in larval and metamorphosed axolotls and in tiger salamanders were determined by electrophoresis on cellulose acetate. In all cases the fastest-migrating component displayed a mobility considerably less than that of frog plasma albumin. An increase in total plasma protein was observed after metamorphosis in axolotls, but not in tiger salamanders. A shift toward an increase in the proportion of the fast-moving component was more apparent in the tiger salamander.

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