Search Results
Search for other papers by A Lafuente in
Google Scholar
PubMed
Search for other papers by J Marcó in
Google Scholar
PubMed
Search for other papers by A I Esquifino in
Google Scholar
PubMed
Abstract
Much is known about the fact that thyrotrophin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulate prolactin secretion but areas of uncertainty remain. This work was undertaken to describe the effects of TRH and VIP on the pulsatile secretion pattern of prolactin, in adult sham-operated and pituitary-grafted hyperprolactinaemic female rats. Two pulses of TRH (1 μg/rat) or one pulse of VIP (20 μg/rat) were given 60 or 120 min after the period of blood sampling. Pituitary grafting increased the mean values of prolactin, absolute amplitude and duration of the peaks and decreased their frequency, compared with control animals. In sham-operated rats, TRH elevated prolactin levels by increasing the absolute and relative amplitudes and duration of the pulses, along with a decrease in their frequency. No priming effects of TRH were observed in this study. Hyperprolactinaemia blunted TRH effects on the pulsatile secretion pattern of prolactin. In sham-operated rats, VIP administration increased the absolute and relative amplitudes of the prolactin peaks. None of the other parameters studied were changed. In pituitary-grafted animals, VIP administration increased the absolute and relative amplitudes of the prolactin peaks but to a lesser extent compared with controls. These data suggest that TRH and VIP affect prolactin pulsatility differentially. The effects of TRH and VIP were blunted to some extent by exposure to previously elevated circulating prolactin levels.
Journal of Endocrinology (1994) 142, 581–586
Search for other papers by KATHLEEN PEASE in
Google Scholar
PubMed
Search for other papers by HIRAM SHEN in
Google Scholar
PubMed
Search for other papers by G. S. ACRES in
Google Scholar
PubMed
Search for other papers by J. H. RUPNOW in
Google Scholar
PubMed
Search for other papers by J. E. DIXON in
Google Scholar
PubMed
SUMMARY
Developmental changes in levels of hypothalamic thyrotrophin releasing hormone (TRH) and the role that hypothalamic degrading enzymes may play in these alterations were investigated. Levels of TRH in male and female fetal rats and in male neonatal rats were measured by radioimmunoassay. The hormone content of the hypothalamus was shown to increase from less than 1 ng at 1–4 days of age to approximately 10 ng at 20 days of age. Thereafter, the content of TRH declined to the adult level of about 5 ng. The ability of fractionated hypothalamic homogenates to degrade TRH was measured over the same time. The 27 000 g supernatant fraction contained a degrading activity that yielded only radiolabelled deamido-TRH upon incubation with [l-proline 2,3-3H]TRH. The corresponding particulate fraction contained at least two distinct TRH degrading activities as determined by the number of metabolites present. Changes in rates of degradation were not large enough to account for the differences observed in levels of TRH.
Search for other papers by M. D. Lewis in
Google Scholar
PubMed
Search for other papers by S. M. Foord in
Google Scholar
PubMed
Search for other papers by M. F. Scanlon in
Google Scholar
PubMed
ABSTRACT
We have developed a fetal rat hypothalamic cell culture system for the study of factors controlling the acute release of TRH. Release of TRH by the cells has been characterized by reversed-phase high pressure liquid chromatography and about 86% of the total immunoreactivity in the medium co-eluted with synthetic TRH. Release of TRH by the cells in response to 56 mmol K+/l increased between days 5 and 9 of culture but reached a plateau thereafter. Cell contents of TRH did not change significantly between days 5 and 14 of culture.
Release of TRH from the cells was stimulated by K+ (56 mmol/l), veratridine (100 μmol/l) and ouabain (100 μmol/l) to 550, 480 and 335% of basal release respectively over a 1-h period. Release of TRH was dependent upon calcium in that it was absent when calcium-free medium was used and could be blocked by verapamil (20 μmol/l); however it could not be blocked by nifedipine (50 μmol/l). The calcium ionophore A23187 (1 μmol/l) stimulated TRH release to 340% of basal release. Tetrodotoxin (1 μmol/l) completely abolished the release in response to veratridine but had no effect on the release stimulated by K+ (56 mmol/l).
The calmodulin antagonists trifluoperazine and triflupromazine (50 μmol/l) inhibited veratridine-stimulated TRH release. This was at a site after calcium influx as they also inhibited A23187-stimulated TRH release. The highly specific calmodulin antagonist W7 (10 μmol/l) also inhibited both veratridine and A23187-stimulated TRH release whereas, at the same concentration, its inactive analogue W5 did not significantly inhibit TRH release in response to either stimulus.
These results confirm that fetal rat hypothalamic cell cultures release authentic TRH which can be stimulated by a number of depolarizing agents. Calcium is essential for depolarization-induced release which is also dependent on calmodulin. Fetal rat hypothalamic cell cultures are a valid model for the study of factors controlling the release of TRH.
J. Endocr. (1987) 115, 255–262
Search for other papers by C. Foltzer-Jourdainne in
Google Scholar
PubMed
Search for other papers by S. Harvey in
Google Scholar
PubMed
Search for other papers by P. Mialhe in
Google Scholar
PubMed
ABSTRACT
Release of GH from perifused duckling hemipituitaries was stimulated, in a biphasic manner, by synthetic TRH and human pancreatic GH-releasing factor (GRF). At all effective concentrations, the level of GH release was increased within 5 min of TRH or GRF perifusion and was maximal after 10 min of TRH perifusion and after 20 min of GRF perifusion. Although TRH was perifused for 20 min the level of GH release declined during the last 10 min. The most effective dose of TRH (1·0 μg/ml; 2·7 μmol/l) and GRF (0·5 μg/ml; 110 nmol/l) provoked similar (250– 300%) increases in the level of GH release. However, since the effect of TRH was only of short duration, the total release of GH induced by GRF was higher than that elicited by TRH, especially with the low dose. The increase in release of GH induced by TRH or GRF was blunted when pituitaries from adult ducks were used. As in young ducks, the GH response to GRF was higher, whereas the response to TRH was very low. The GH response of perifused adult pituitaries to GRF was, however, potentiated when TRH was perifused simultaneously. The basal release of GH from both young and adult pituitary glands was unaffected by perifusion with somatostatin-14 (SRIF-14) at doses of 1 and 2 μg/ml. The perifusion of hemipituitary glands with similar doses of SRIF-14 was also unable to suppress the stimulation of GH release induced by prior perifusion with GRF, although when SRIF-14 and TRH were simultaneously perifused TRH-induced GH release was markedly suppressed.
These results demonstrate direct effects and interactions of TRH, GRF and SRIF on the release of GH from duck pituitary glands. GRF is the most potent releasing factor for GH in both young and adult ducks although in adult ducks it is less effective. These results also provide evidence that the age-related decline in the in-vivo GH response to TRH is due to a desensitization of pituitary somatotrophs.
J. Endocr. (1988) 119, 421–429
Search for other papers by M. Mori in
Google Scholar
PubMed
Search for other papers by M. Yamada in
Google Scholar
PubMed
ABSTRACT
The negative-feedback action of thyroid hormones on TRH in the hypothalamic median eminence was examined. Thyroidectomy caused a progressive decrease in TRH content of the median eminence, but not of the whole hypothalamus. In contrast, it did not affect the LHRH content of the median eminence. Administration of thyroid hormone prevented the decrease in TRH content of the median eminence after thyroidectomy. Destruction of the hypothalamic paraventricular nucleus (PVN) led to a significant reduction in TRH content of the median eminence in normal and thyroidectomized rats. These data provide evidence that thyroid hormones regulate directly the amount of median eminence TRH which is derived from the hypothalamic PVN in the rat.
J. Endocr. (1987) 114, 443–448
Search for other papers by A. M. Horn in
Google Scholar
PubMed
Search for other papers by H. M. Fraser in
Google Scholar
PubMed
Search for other papers by G. Fink in
Google Scholar
PubMed
ABSTRACT
The possible role of thyrotrophin-releasing hormone (TRH) in causing the pro-oestrous surge of prolactin was investigated in conscious female rats by passive immunization with a specific anti-TRH serum raised in sheep. Blood samples were withdrawn through a previously implanted intra-atrial cannula. The i.p. injection of 1 ml anti-TRH serum, but not non-immune sheep serum, at 13.00 h of pro-oestrus delayed by about 1 h the onset of the prolactin surge, but the peak of the surge was similar to that in animals injected with the non-immune serum. The plasma concentrations of TSH were significantly reduced by the anti-TRH serum, but plasma concentrations of LH were not significantly affected. These results show that TRH may play an important role in the timing and initiation, but not the maintenance of the prolactin surge in the pro-oestrous rat.
J. Endocr. (1985) 104, 205–209
Search for other papers by G. M. BESSER in
Google Scholar
PubMed
Search for other papers by J. G. RATCLIFFE in
Google Scholar
PubMed
Search for other papers by J. R. KILBORN in
Google Scholar
PubMed
Search for other papers by B. J. ORMSTON in
Google Scholar
PubMed
Search for other papers by R. HALL in
Google Scholar
PubMed
SUMMARY
Thyrotrophin (TSH) release in response to intravenous synthetic thyrotrophin releasing hormone (TRH) was unaltered by simultaneous corticotrophin (ACTH) and growth hormone secretion induced by hypoglycaemia or methylamphetamine in normal subjects. Secretion of growth hormone was the same whether or not TSH was secreted. While the increments in plasma corticosteroids and ACTH after methylamphetamine administration were not different whether TRH or a control injection was given, they rose more during insulin-induced hypoglycaemia when TRH was given as well. This could have been due to a slightly greater degree of stress after TRH + insulin than insulin alone. Overnight dexamethasone suppression of basal ACTH secretion did not alter the TSH response to TRH. Unlike the rat, there is no evidence suggesting competition between pituitary mechanisms involved in ACTH, growth hormone and TSH release in man.
Search for other papers by A. D. TOFT in
Google Scholar
PubMed
Search for other papers by A. R. BOYNS in
Google Scholar
PubMed
Search for other papers by E. N. COLE in
Google Scholar
PubMed
Search for other papers by W. J. IRVINE in
Google Scholar
PubMed
Thyrotrophin releasing hormone (TRH) is a potent stimulus of the release of thyrotrophin (TSH) and prolactin from the anterior pituitary gland of man (Bowers, Friesen, Hwang, Guyda & Folkers, 1971; Jacobs, Snyder, Wilber, Utiger & Daughaday, 1971; L'Hermite, Vanhaelst, Copinschi, Leclercq, Golstein, Bruno & Robyn, 1972; Toft, Boyns, Cole, Groom, Hunter & Irvine, 1973). Whereas the plasma TSH response to intravenous TRH is enhanced in patients with primary hypothyroidism, and abolished in patients with thyrotoxicosis, the relationship between thyroid status and prolactin release by TRH is not clear. Although there is a small increase in plasma prolactin in hypothyroidism (Jacobs et al. 1971; Toft et al. 1973) the response to TRH is not significantly different from that seen in normal subjects (Toft et al. 1973). Recently, Snyder, Jacobs, Utiger & Daughaday (1973) found that when patients with thyroid disease were studied before and after treatment, the prolactin response to TRH
Search for other papers by J. Domin in
Google Scholar
PubMed
Search for other papers by J. H. Steel in
Google Scholar
PubMed
Search for other papers by N. Adolphus in
Google Scholar
PubMed
Search for other papers by J. M. Burrin in
Google Scholar
PubMed
Search for other papers by U. Leonhardt in
Google Scholar
PubMed
Search for other papers by J. M. Polak in
Google Scholar
PubMed
Search for other papers by S. R. Bloom in
Google Scholar
PubMed
ABSTRACT
In this study we have examined the effects of TRH, thyroid hormones and dopamine on the rat anterior pituitary content of neuromedin U-like immunoreactivity. Oral administration of TRH (20 mg/100 g per day) to euthyroid animals evoked a fivefold increase in peptide content after 12 days of treatment. This effect was found to be dependent upon circulating levels of thyroid hormone, since administration of TRH to thyroidectomized animals failed to show a similar effect without simultaneous treatment with tri-iodothyronine. The possibility that the TRH-induced increase in anterior lobe neuromedin U content reflected alterations in prolactin secretion or synthetic rate was also examined. Treatment of euthyroid animals with a dopamine agonist and antagonist was, however, without effect. These results demonstrate a unique relationship between TRH and thyroid hormone levels in increasing the anterior lobe content of neuromedin U immunoreactivity.
Journal of Endocrinology (1989) 122, 471–476
Search for other papers by C. OLIVER in
Google Scholar
PubMed
Search for other papers by C. R. PARKER JR in
Google Scholar
PubMed
Search for other papers by J. C. PORTER in
Google Scholar
PubMed
*Laboratoire de Médecine Expérimentale, UER Médecine Nord, Boulevard Pierre Dramard, 13326 Marseille Cedex 3, France and †Department of Obstetrics and Gynecology, Southwestern Medical School, 5323 Harry Hines Boulevard, Dallas, Texas 75235, U.S.A.
(Received 15 March 1977)
Thyrotrophin releasing hormone (TRH) is rapidly degraded when incubated at 37 °C with plasma (Redding & Schally, 1969) or brain homogenates (Bassiri & Utiger, 1974) from adult rats. However, immunoreactive TRH is stable in serum obtained from rats less than 2 weeks old (Oliver, Taurog & Porter, 1974). No loss of biological or immunological TRH activity occurs during incubation with serum from 4- or 16-day-old rats (Neary, Kieffer, Federico, Mover, Maloof & Soodak, 1976). In this report, we have determined the TRH degrading activity of brain homogenates and serum obtained from male rats at various stages of development after birth.
Synthetic TRH (1 ng, Beckman Instruments, Inc.) diluted in 50 μl phosphate-buffered saline (0·01
