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Research Article Free access | 10.1172/JCI108955

The Physiological Role of Thyrotropin-Releasing Hormone in the Regulation of Thyroid-Stimulating Hormone and Prolactin Secretion in the Rat

Arthur R. C. Harris, Dana Christianson, M. Susan Smith, Shih-Lieh Fang, Lewis E. Braverman, and Apostolos G. Vagenakis

Department of Endocrinology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

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Department of Endocrinology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

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Department of Endocrinology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

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Department of Endocrinology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

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Department of Endocrinology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

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Department of Endocrinology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01605

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Published February 1, 1978 - More info

Published in Volume 61, Issue 2 on February 1, 1978
J Clin Invest. 1978;61(2):441–448. https://doi.org/10.1172/JCI108955.
© 1978 The American Society for Clinical Investigation
Published February 1, 1978 - Version history
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Abstract

The physiological role of thyrotropin-releasing hormone (TRH) in the regulation of thyrotropin (thyroid-stimulating hormone, TSH) and prolactin (Prl) secretion has been assumed but not proven. Stimulation of their release requires pharmacologic doses of TRH. Lesions of the hypothalamus usually induce an inhibition of TSH secretion and an increase in Prl. To determine whether TRH is essential for TSH and Prl secretion in the rat, 0.1 ml of TRH antiserum (TRH-Ab) or normal rabbit serum was administered to normal, thyroidectomized, cold-exposed, and proestrus rats through indwelling atrial catheter. Serum samples were obtained before and at frequent intervals thereafter. Serum TSH concentrations in normal, thyroidectomized, cold-exposed, and proestrus rats were not depressed in specimens obtained up to 24 h after injection of normal rabbit serum. In contrast, serum TSH was significantly decreased after the administration of TRH-Ab in all normal (basal, 41±8 μU/ml [mean±SE]; 30 min, 6±2; 45 min, 8±3; 75 min, 4±2); thyroidectomized (basal, 642±32 μU/ml; 30 min, 418±32; 60 min, 426±36; 120 min, 516±146); coldstressed (basal, 68±19 μU/ml; 30 min, 4±3; 180 min, 16±8); and proestrus (basal, 11 a.m., 57±10 μU/ml; 1 p.m., 20±3; 3 p.m., 13±4; 5 p.m., 19±3) rats. However, 0.1 ml of TRH-Ab had no effect on basal Prl concentrations in normal or thyroidectomized rats and did not prevent the Prl rise in rats exposed to cold (basal, 68±7 ng/ml; 15 min, 387±121; 30 min, 212±132; 60 min, 154±114), or the Prl surge observed on the afternoon of proestrus (basal 11 a.m., 23±2 ng/ml; 1 p.m., 189±55; 3 p.m., 1,490±260; 5 p.m., 1,570±286). These studies demonstrate that TRH is required for TSH secretion in the normal, cold-exposed and proestrus rat and contributes, at least in part, to TSH secretion in the hypothyroid rat, but is not required for Prl secretion in these states.

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