Studies of pituitary and thyroid function were conducted in adult rats with the syndrome of neonatal thyrotoxicosis (NT) produced by the administration of large doses of L-thyroxine during the first week of postnatal life. As compared to normal controls,adult NT rats displayed decreased thyroid ^I31I uptake, an increase in the proportion ofthyroid organic ¹³¹I present as monoiodotyrosine and a decreased proportion of the iodothyronines,thyroxine (T₄)and triiodothyronine, findings consis-)tent with those seen in association with deficiency of TSH. In addition,serum T₄ concentrations were consistently lower in adult NT than in control rats.

Adult NT rats displayed marked decreases in TSH secretory reserve, as indicated by lower values of basal serum TSH concentration following thyroidec-tomy and far lower increments in serum TSH concentration following standard doses of TRH iv, even when NT and control rats had all been thyroidectomized and maintained for long periods on replacement doses of L-thyroxine.

Abnormalities in thyroid ¹³¹I uptake,serum T₄ concentration, and pituitary TSH secretory reserve comparable to those seen in NT rats were not displayed by adult rats deprived of food during the first week of life to an extent sufficient to retard growth to anextent equal to that seen in NT rats during this period.

It is concluded that the syndrome of NT in the adult rat is the result of thyroid hormone excess, rather than caloric insufficiency, during the neonatal period, that it is characterized by thyroid hypofunc-tion secondary to decreased TSH secretion, and that a defect in TSH secretion is the probable primary cause of the thyroid aspect of the syndrome. (Endocrinology94: 1681, 1974)