scholarly journals Effect of continuous infusion of thyrotrophin-releasing hormone on plasma prolactin and on ovarian activity in melatonin-treated ewes

Reproduction ◽  
1996 ◽  
Vol 107 (1) ◽  
pp. 17-22 ◽  
Author(s):  
J. J. Robinson ◽  
R. P. Aitken ◽  
T. Atkinson ◽  
J. M. Wallace ◽  
A. S. McNeilly
Keyword(s):  
Continuous Infusion ◽  
Ovarian Activity ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

THYROTROPHIN RELEASING HORMONE-INDUCED GROWTH HORMONE AND PROLACTIN RELEASE: PHYSIOLOGICAL STUDIES IN INTACT RATS AND IN HYPOPHYSECTOMIZED RATS BEARING AN ECTOPIC PITUITARY GLAND

1977 ◽  
Vol 72 (3) ◽  
pp. 301-311 ◽  
Author(s):  
A. E. PANERAI ◽  
IRIT GIL-AD ◽  
DANIELA COCCHI ◽  
V. LOCATELLI ◽  
G. L. ROSSI ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Time Lapse ◽  
Anterior Pituitary Gland ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Clear Cut ◽  
Urethane Anaesthesia ◽  
Releasing Effect

SUMMARY To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0·15 and 0·6 μg) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3, 8,15, 30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16·0 ng/ml (1 day) to about 3·0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0·15 μg), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85·0 ng/ml (1 day) to about 32·0 ng/ml (8 days); subsequently (15–60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0·6 μg TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1·2 μg while a short-lived but clear-cut prolactin response could be obtained even with the 0·3 μg dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin-than GH-releaser on the pituitary gland in situ.

Effects of infusion of thyrotrophin releasing hormone and dopamine either alone or in combination on plasma prolactin concentrations in the anoestrous ewe

1983 ◽  
Vol 96 (2) ◽  
pp. 353-357
Author(s):  
B. F. Fitzgerald ◽  
F. J. Cunningham
Keyword(s):  
Combined Treatment ◽  
Plasma Concentrations ◽  
Regulatory Role ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

Plasma concentrations of prolactin in anoestrous ewes were respectively lowered or raised by the separate infusion of dopamine or thyrotrophin releasing hormone (TRH). Combined treatment with dopamine and TRH lowered the concentration of prolactin in plasma but the values increased markedly after the treatment was stopped and reached a level equivalent to that found in ewes treated with TRH alone. The results are interpreted as evidence that both dopamine and TRH play a regulatory role in determining the secretion of prolactin in the ewe.

EVIDENCE FOR THE INVOLVEMENT OF HYPOTHALAMIC DOPAMINE AND THYROTROPHIN-RELEASING HORMONE IN SUCKLING-INDUCED RELEASE OF PROLACTIN

1981 ◽  
Vol 91 (2) ◽  
pp. 213-223 ◽  
Author(s):  
W. J. DE GREEF ◽  
T. J. VISSER
Keyword(s):  
Nerve Stimulation ◽  
Plasma Levels ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Dopamine Infusion ◽  
Releasing Hormone ◽  
Peripheral Plasma ◽  
Transient Decrease ◽  
Hypothalamic Dopamine

The changes in adenohypophysial and hypothalamic content and in hypothalamic release of dopamine and thyrotrophin-releasing hormone (TRH) into the hypophysial portal system during the suckling-induced release of prolactin were investigated. An increase in peripheral plasma levels of prolactin was induced by mammary nerve stimulation in urethane-anaesthetized and by suckling in unanaesthetized lactating rats. In the unanaesthetized rat, suckling caused a decrease of dopamine levels in hypothalamus and adenohypophysis and a short-lasting small increase in hypothalamic TRH. Mammary nerve stimulation induced a transient decrease in dopamine levels and an increase in TRH levels in hypophysial stalk blood. To assess the significance of the observed changes in dopamine and TRH levels for prolactin release, these changes in dopamine and TRH were mimicked in lactating rats anaesthetized with urethane and pretreated with α-methyl-p-tyrosine (AMpT, a competitive inhibitor of catecholamine synthesis). Reducing hypothalamic dopamine secretion by treatment with AMpT increased peripheral plasma levels of prolactin from 15 to 477 ng/ml; an infusion with dopamine, resulting in plasma levels similar to those measured in hypophysial stalk plasma, reduced plasma levels of prolactin to 127 ng/ml. Neither a 50% reduction in dopamine infusion rate for 15 min nor administration of 100 ng TRH caused an appreciable change in plasma prolactin levels. However, when dopamine infusion was reduced by 50% for 15 min just before TRH was injected, then an increase in plasma levels of prolactin from 172 to 492 ng/ml was observed. Thus, the effectiveness of TRH in releasing prolactin in the lactating rat was enhanced when a transient decrease of dopamine levels occurred before treatment with TRH. It is concluded that the changes observed in dopamine and TRH levels in hypophysial stalk blood are involved in the suckling-induced prolactin release in an important manner.

Effects of antiserum to thyrotrophin-releasing hormone on the concentrations of plasma prolactin, thyrotrophin and LH in the pro-oestrous rat

1985 ◽  
Vol 104 (2) ◽  
pp. 205-209 ◽  
Author(s):  
A. M. Horn ◽  
H. M. Fraser ◽  
G. Fink
Keyword(s):  
Plasma Concentrations ◽  
Passive Immunization ◽  
Immune Serum ◽  
Female Rats ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Blood Samples ◽  
Releasing Hormone ◽  
Sheep Blood

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

INFLUENCE OF SUCKLING AND OF SUCKLING FOLLOWED BY TRH OR LH-RH ON PLASMA PROLACTIN, TSH, GH AND FSH

1976 ◽  
Vol 82 (1) ◽  
pp. 246-253 ◽  
Author(s):  
S. Jeppsson ◽  
K. O. Nilsson ◽  
G. Rannevik ◽  
L. Wide
Keyword(s):  
Limit Of Detection ◽  
Post Partum ◽  
Prolactin Secretion ◽  
Plasma Prolactin ◽  
Additional Increase ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Before And After ◽  
Plasma Gh ◽  
Lh Rh

ABSTRACT Ten women were studied during the first post-partum week. Suckling for 20 min induced a marked increase in plasma prolactin, reaching a maximum within 0–25 min after the end of suckling and then returning to pre-suckling levels after 120 min. Suckling induced no changes in plasma thyrotrophin (TSH), growth hormone (GH) or follicle stimulating hormone (FSH). The iv injection of 200 μg of thyrotrophin releasing hormone (TRH) immediately after suckling resulted in an additional increase in plasma prolactin and a rise in TSH. When given 120 min after suckling TRH was followed by increased plasma levels of prolactin and TSH, which for both hormones were of a magnitude comparable to the TRH induced increment seen immediately after suckling. Thus, suckling did not inhibit the effect of TRH on the release of TSH. These studies indicate that TRH is probably not involved in the suckling induced increase in prolactin secretion. The mean plasma FSH level was below the limit of detection before and after suckling. Neither plasma FSH nor prolactin showed any appearant changes following the iv injection of 25 μg of luteinizing hormone releasing hormone (LH-RH), when given immediately after and 120 min after suckling. When given after suckling as indicated above, TRH induced no changes in plasma GH or FSH and similarly LH-RH was without influence on plasma GH and TSH.

scholarly journals Thyrotrophin-releasing hormone receptor 1 and prothyrotrophin-releasing hormone mRNA expression in the central nervous system are regulated by suckling in lactating rats

2005 ◽  
Vol 152 (5) ◽  
pp. 791-803 ◽  
Author(s):  
Åse-Karine Fjeldheim ◽  
Per Ivar Høvring ◽  
Ole-Petter Løseth ◽  
Per Wiik Johansen ◽  
Joel C Glover ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mrna Expression ◽  
Physiological Role ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Central Nervous System ◽  
Plasma Prl

Background: The accepted function of the hypothalamic peptide, thyrotrophin-releasing hormone (TRH), is to initiate release of thyrotrophin (TSH) from the pituitary. A physiological role for TRH in lactating rats has not yet been established. Methods: Tissues were prepared from random-cycling and lactating rats and analysed using Northern blot, real time RT-PCR and quantitative in situ hybridisation. Results: This study demonstrates that TRH receptor 1 (TRHR1) mRNA expression is up-regulated in the pituitary and in discrete nuclei of the hypothalamus in lactating rats, while proTRH mRNA expression levels are increased only in the hypothalamus. The results were corroborated by quantitative in situ analysis of proTRH and TRHR1. Bromocriptine, which reduced prolactin (PRL) concentrations in plasma of lactating and nursing rats, also counteracted the suckling-induced increase in TRHR1 mRNA expression in the hypothalamus, but had an opposite effect in the pituitary. These changes were confined to the hypothalamus and the amygdala in the brain. Conclusions: The present study shows that the mechanisms of suckling-induced lactation involve region-specific regulation of TRHR1 and proTRH mRNAs in the central nervous system notably at the hypothalamic level. The results demonstrate that continued suckling is critical to maintain plasma prolactin (PRL) levels as well as proTRH and TRHR1 mRNA expression in the hypothalamus. Increased plasma PRL levels may have a positive modulatory role on the proTRH/TRHR1 system during suckling.

Effect of immunoneutralization of thyrotrophin-releasing hormone on the release of thyrotrophin and prolactin during suckling or in response to electrical stimulation of the hypothalamus in the anaesthetized rat

1985 ◽  
Vol 106 (1) ◽  
pp. 113-119 ◽  
Author(s):  
W. J. Sheward ◽  
H. M. Fraser ◽  
G. Fink
Keyword(s):  
Electrical Stimulation ◽  
Neural Control ◽  
Brain Area ◽  
Plasma Concentrations ◽  
Female Rats ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Prolactin Response ◽  
Stimulation Of

ABSTRACT The aim of the present study was to use the technique of immunoneutralization with anti-thyrotrophin-releasing hormone (anti-TRH) serum to investigate the role of TRH in mediating the TSH and prolactin responses to electrical stimulation of the hypothalamus and the prolactin response to suckling in lactating rats. Electrical stimulation of either the median eminence or paraventricular nuclei of male or female rats anaesthetized with urethane resulted in significant increases in the plasma concentrations of both TSH and prolactin. Injection of sheep anti-TRH serum blocked the rise in plasma TSH concentration in response to stimulation of either brain area, but did not block the increase in plasma prolactin concentration. In anaesthetized, lactating female rats, the suckling stimulus produced a significant increase in the plasma prolactin concentration, but did not alter the plasma TSH concentration. Injection of anti-TRH serum, but not control non-immune or anti-bovine serum albumin, significantly decreased the basal release of TSH but did not abolish the prolactin response to suckling. These results show that TRH is the principal mediator of the neural control of TSH release in the rat, but is not crucial for the release of prolactin in response to either hypothalamic stimulation or suckling. J. Endocr. (1985) 106, 113–119

Study of prolactin levels in the ferret

1983 ◽  
Vol 99 (3) ◽  
pp. 415-421 ◽  
Author(s):  
S. V. Smith ◽  
I. A. Forsyth ◽  
B. T. Donovan
Keyword(s):  
Luteinizing Hormone ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Standard Curve ◽  
Pituitary Glands ◽  
Serial Dilutions

A radioimmunoassay for canine prolactin has been used to measure prolactin in the ferret. Serial dilutions of extracts of ferret pituitary glands and of ferret plasma yielded curves that were parallel with the canine prolactin standard curve. The sensitivity, accuracy, reproducibility and precision of the assay were within acceptable limits. Plasma prolactin levels increased after the administration of thyrotrophin releasing hormone (TRH) or chlorpromazine, but not after giving luteinizing hormone releasing hormone. Female ferrets, which were anoestrous, oestrous or spayed, and male ferrets had similar basal prolactin levels when sampled under sodium pentobarbitone anaesthesia. These basal levels were higher than in conscious males and the latter also showed a lesser response to TRH. Hypophysectomy significantly reduced basal prolactin levels in female ferrets by 2 h postoperatively and abolished the response to TRH.

Pro-oestrous-specific role for polyamines in mediating the secretion of prolactin induced by thyrotrophin-releasing hormone in the rat

1993 ◽  
Vol 137 (1) ◽  
pp. 133-139 ◽  
Author(s):  
G. A. Wynne-Jones ◽  
A. M. Gurney
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Anterior Pituitary Gland ◽  
Oestrous Cycle ◽  
Male Rats ◽  
Pituitary Cells ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

ABSTRACT The activity of ornithine decarboxylase (ODC) in the rat anterior pituitary gland varies during the oestrous cycle, with a rise in activity seen at pro-oestrus. This enzyme, which is rate-limiting for the synthesis of the polyamines, can be specifically and irreversibly blocked by α-difluoromethylornithine (DFMO). A previous study showed that when this drug was administered to rats in vivo on the afternoon of pro-oestrus, it suppressed the normal surge in plasma prolactin levels that occurred later that day. The effect of DFMO was associated with reduced levels of putrescine in the anterior pituitary gland, suggesting that ODC activity in the lactotroph might be involved in the prolactin surge. We have examined the effects of DFMO on the secretion of prolactin from anterior pituitary cells, isolated either from male rats or from females at different stages of the oestrous cycle. The drug was found to reduce prolactin secretion stimulated by thyrotrophin-releasing hormone (TRH), but only in cells isolated from pro-oestrous animals and only for 2 days after cell isolation. Basal secretion was unaffected by DFMO. The results imply that ODC is important for TRH-stimulated prolactin secretion at pro-oestrus, and it is specific for pro-oestrus. The prolactin surge could therefore be influenced by this ODC-dependent effect of TRH. The pro-oestrous-specific response to TRH may be a consequence of the increased ODC activity seen at this time. Alternatively, the increased ODC activity could be a consequence of coupling to TRH receptors, which are known to increase in number at pro-oestrus. Journal of Endocrinology (1993) 137, 133–139

Sign in / Sign up

Export Citation Format

Share Document