The ultrastructure of the thyrotropic cell during thyrotropin rebound in the adenohypophysis of the rat

Authors


  • Supported, in part, by grant AM-00432 and a Career Research Award given to Dr. S. A. D'Angelo by the NIH: and by PHS General Research Support grant RR-5414.

Abstract

Adenohypophyses of rats were studied ultrastructurally to ascertain the morphologic changes that occur in thyrotropic cells during the pituitary TSH Rebound Phenomenon. Rats were maintained on propylthiouracil (PTU) for 43–147 days and their adenohypophyses studied three to nine days after discontinuance of goitrogen treatment. TSH rebound was also induced in chronically hypothyroid rats by single intravenous injections of 0.8, 4, 20 and 200 μg of thyroxine. Pituitaries were studied from animals sacrificed 6–24 hours after thyroxine injection. Thyrotrophs of euthyroid rats were characterized ultrastructurally by the presence of numerous peripherally-located, small secretory granules (storage phase) and by highly dilated cisternae of rough endoplasmic reticulum (secretory phase). The thyrotropic cells in PTU-treated rats were sparsely granulated, displayed enlarged mitochondria with much loss of cristae and contained extensively dilated rough endoplasmic reticulum and expanded Golgi membranes.

Marked repletion of granules, both intracisternal and cytoplasmic, was seen during TSH rebound in the pituitary. It was observed in some thyrotrophs as early as three days after goitrogen withdrawal and was enhanced further at the 6- and 9-day intervals. Granule repletion increased progressively with doses of thyroxine up to 20 μg and assayable thyrotropin in pituitary glands increased 500–700% over normal. Effects with the 20 μg dose could be detected as early as six hours. With higher doses of thyroxine, granule repletion in thyrotrophs was inhibited and mitcohondrial hypertrophy was largely reversed.

The electron microscopic findings reveal close correlation with previously published data on thyrotropin assays of the rat pituitary. They support the concept that the degree of cytoplasmic granulation in thyrotropic cells is quantitatively related to assayable stores of thyrotropin in the anterior pituitary gland.

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