EFFECTS OF HYPOTHALAMIC LESIONS AND SUBSEQUENT PROPYLTHIOURACIL TREATMENT ON PITUITARY STRUCTURE AND FUNCTION IN THE RAT<sup>1</sup>

Bogdanove, E. M.; Halmi, N. S.

doi:10.1210/endo-53-3-274

Cited by 85 publications

(26 citation statements)

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“…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).…”

Section: Introductionmentioning

confidence: 99%

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

Theodoropoulos¹,

Braverman²,

Vagenakis³

1979

J. Clin. Invest.

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A B S T R A C T To determine the role of thyrotropinreleasing hormone (TRH) in the regulation of thyroidstimulating hormone (TSH) secretion in the perinatal period, a physiological approach of neutralizing circulating TRH in the fetal andl early neonatal rat was employed. TRH-antiserum (TRH-AS) raised in rabbits and administered daily to low iodine-propylthiouracil (LID-PTU)-fed pregnant rats from days 12 to 19 of gestation markedly impaired the rise in serum TSH to LID-PTU when compared with normal rabbit serumtreated controls. In contrast, fetal serum TSH was unaffected by TRH-AS. The binding capacity of TRH-AS in the fetal serum (111 ng/iiil) far exceeded circulating TRH in the fetus. Similarly7, acute TRH-AS administration to the pregnant rat fed LID-PTU markedly decreased the serum TSH concentration in the mother, but not in the fetus, 60 niin after TRH-AS administration. Chronic TRH-AS administration to neonatal rats whose nursing mothers were fed LID-PTU was ineffective in decreasing the elevated serum TSH in the neonate through day 8 of life, whereas a slight but significant decrease in serum TSH was observed on day 10. Chronic daily TRH-AS administration to neonatal rats through day 10 of life had no effect on the later development of the hypothalamic-pituitary-thyroid axis. These findings suggest that TRH does not participate in TSH regulation during the perinatal life in the rat and that thyroid hormones are probably the main regulators of TSH secretion during this period.Placental TRH is niot importanit in regulating TSH secretion in the fetal rat. Furthermore, TRtH "deprivation" during neonatal life does not prevent normal later developmenit of the hypothalamic-pituitarythyroid axis.

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Section: Introductionmentioning

confidence: 99%

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

Theodoropoulos¹,

Braverman²,

Vagenakis³

1979

J. Clin. Invest.

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“…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.…”

Section: Introductionmentioning

confidence: 99%

“…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 INTRODUCTION The 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)(2)(3)(4)(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.…”

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confidence: 99%

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

Harris¹,

Christianson²,

Smith³

et al. 1978

J. Clin. Invest.

119

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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...

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“…The consensus of opinion from such earlier accounts is that pars intermedia undergoes hypertrophy, and in some cases hyperplasia, following these experimental procedures. In the course of some studies in the rat on the central nervous control of the adenohypophysis, involving damage to the hypothalamus, Bogdanove & Halmi (1953) briefly reported similar changes in the pars intermedia, which they described as hyperplasia. However, since the authors unfortunately gave no details concerning the site of their lesions, it is not known whether the same hypothalamic area was involved in their investigation as in the present experiments.…”

Section: +4115mentioning

confidence: 95%

The effect of hypothalamic lesions on the melanocyte‐stimulating hormone content and histology of the pars intermedia of the rat pituitary gland

Howe¹,

Thody²

1969

The Journal of Physiology

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SUMMARY1. The effect of bilateral lesions in the anterior hypothalamus on the histology and content of melanocyte-stimulating hormone (MSH) of the pars intermedia has been studied in the adult male rat.2. By 7-15 days striking histological changes, suggestive of hyperactivity, were evident. These changes were accompanied by an elevated MSH content, which was particularly noticeable at 7 days.3. By 7 days there was an increase in the acid phosphatase activity of pars intermedia cells, as demonstrated histochemically.4. It was concluded that a hypothalamic control system exists for the mammalian pars intermedia and may involve both inhibitory and excitatory components.

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EFFECTS OF HYPOTHALAMIC LESIONS AND SUBSEQUENT PROPYLTHIOURACIL TREATMENT ON PITUITARY STRUCTURE AND FUNCTION IN THE RAT¹

Cited by 85 publications

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

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

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

The effect of hypothalamic lesions on the melanocyte‐stimulating hormone content and histology of the pars intermedia of the rat pituitary gland

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EFFECTS OF HYPOTHALAMIC LESIONS AND SUBSEQUENT PROPYLTHIOURACIL TREATMENT ON PITUITARY STRUCTURE AND FUNCTION IN THE RAT1

Cited by 85 publications

References 0 publications

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

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

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

The effect of hypothalamic lesions on the melanocyte‐stimulating hormone content and histology of the pars intermedia of the rat pituitary gland

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Product

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EFFECTS OF HYPOTHALAMIC LESIONS AND SUBSEQUENT PROPYLTHIOURACIL TREATMENT ON PITUITARY STRUCTURE AND FUNCTION IN THE RAT¹