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

Abstract

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...

Thyrotropin-Releasing Hormone is not Required for Thyrotropin Secretion in the Perinatal Rat

“…Control rats were injected with 0.3 ml normal rabbit serum (NRS). The TRH-AS employed in these experiments displayed a binding capacity of 48 nM/liter and when used in the TRH radioimmunoassay in a dilution of 1:50,000, 30% of [1251]TRH was bound to antiserum (6). Blood was obtained by heart puncture from the pregnant rats under light ketamine anaesthesia, the fetuses were removed through cesarian section, and fetal blood was collected from the trunk, after decapitation.…”

“…Evidence for the TRH control of TSH seiLretion has been derived mainly from animal studies with hypothalamic lesions, basal hypothalamic deaffereintation, or heterotopic pituitary transplantation, all of which result in a decrease in pituitary TSH secretion (1)(2)(3)(4)(5). Recently, we and others (6)(7)(8) have reported that passive immunization with TRH' antibody results in a marked decrease in the basal and cold-stimulated TSH secretion in the normal and hypothyroid adult riat, although the role of endogenous TRH in maintaining increased serum TSH in the hypothyroid rat has been questioned (9).…”

Thyroid hormone metabolism in innate immune cells

“…the hypothalamic-pituitary-thyroid (HPT) axis. Hypophysiotropic neurons within the paraventricular nucleus of the hypothalamus produce thyrotropinreleasing hormone (TRH), which in turn stimulates the thyrotroph cells of the anterior pituitary to synthesize and secrete thyroid-stimulating hormone (TSH) (Harris et al 1978). TSH then stimulates the thyroid gland to produce thyroid hormones in the form of thyroxine (T 4 ) and triiodothyronine (T 3 ) (Miot et al 2015).…”

Efficient non-viral transfection of adult neural stem/progenitor cells, without affecting viability, proliferation or differentiation

“…Thyrotropin-releasing hormone (TRH) is produced in the paraventricular nucleus of the hypothalamus 111 and stimulates the secretion of thyroid-secreting hormone (TSH) from the anterior pituitary 112,113 . TSH in turn regulates the biosynthesis and release of thyroid hormone 114 .…”