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Studies were carried out on various aspects of hypothalamic-pituitary-thyroid function in normal and gonadectomized adult male and female rats. Consistent increases in the serum TSH concentration and the serum TSH response to TRH were observed in the male rat compared to values in the female. Orchiectomy induced a decrease in the serum TSH concentration and the serum TSH response to TRH, and these functions were equal in gonadectomized male and female rats. Oophorectomy did not affect basal and TRH-stimulated serum TSH concentrations. Replacement doses of testosterone (0.33 mg/day) to orchiectomized rats increased and restored these values to those observed in the normal male rat, while replacement doses of estradiol (0.33 microgram/day) to the oophorectomized rat had no effect on basal or TRH-stimulated TSH concentrations. No sex-related differences in pituitary TSH and hypothalamic TRH contents or in serum T4 and T3 concentrations were observed. The present studies strongly suggest that the increased TSH responsiveness observed in male compared to female rats is due to the presence of testosterone. (Endocrinology 108: 529, 1981)

A B S T R A C T The physiological role of thyrotropinreleasing 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 AU/ml [mean±SE]; 30 min, 6+-2; 45 min, 8+3; 75 min, 4±2); thyroidectomized (basal, 642+32 ,uU/ml; 30 min, 418±32; 60 min, 426±36; 120 min, 516±146); coldstressed (basal, 68±19 uU/ml; 30 min, 4±3; 180 min, 16±8); and proestrus (basal, 11 a.m., 57±10,U/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. INTRODUCTIONThe administration of pharmacologic doses of thyrotropin-releasing hormone (TRH)' has been demonstrated to stimulate thyrotropin (thyroid-stimulating hormone, TSH) and prolactin (Prl) synthesis and release from the anterior pituitary (1-5). Surgical or pathologic lesions ofthe hypothalamus have resulted in decreased TSH release and subsequent hypothyroidism (6)(7)(8)(9)(10). It is well established that Prl secretion is tonically suppressed by dopamine either by a direct effect on the pituitary or by modulating the release of the Prl inhibiting factor. Median eminence and pituitary stalk lesions usually enhance rather than suppress Prl secretion (11,12), although this is not always observed in unstressed rats after hypothalamic deafferentation (13). In intact animals, electrical stimulation of the hypothalamic "hypophysiotropic area" (14) has been shown to increase serum TSH levels (10,15), presumably secondary to TRH release, although direct experimental evidence of enhanced TRH release is lacking. The effect of such electrical stimulation on Prl secretion is variable (16). The alterations in TSH or Prl release after hypothalamic lesion...

In order to determine whether T4, TSH, or both affect hypothalamic TRH content, primary or secondary hypothyroidism was induced in the rat by thyroidectomy (Tx) or hypophysectomy (Hx), respectively. Two weeks later, rats were treated with T4, TSH, or both for 14--16 days. Tx or Hx significantly decreased hypothalamic TRH content, and T4 treatment restored hypothalamic TRH to normal in the Tx but not in the Hx rats. When TSH was administered simultaneously with T4 to Hx rats, hypothalamic TRH content was restored to normal. Whole brain TRH content was not affected by Tx, Hx, or by the various treatment regimens. Similar experiments were performed in Snell dwarf (dw/dw) mice. Hypothalamic TRH content was significantly decreased when compared to normal litter mates (dw/+). As in Hx rats, T4 administration to dw/dw mice for 16 days did not restore hypothalamic TRH content to normal. Brain TRH content was similar in both groups and was not altered by T4 treatment. It is concluded that T4 affects hypothalamic TRH content, but that TSH is required for this T4 effect. Whole brain TRH, on the other hand, is unaffected by any of these alterations in thyroid-pituitary function.

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