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 Blood samples were withdrawn through a previously implanted intra-atrial cannula.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

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

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.

scholarly journals Intracerebroventricular administration of the prolactin (PRL) receptor antagonist, S179D PRL, disrupts parturition in rats

Reproduction ◽  
2007 ◽  
Vol 134 (1) ◽  
pp. 155-160 ◽  
Author(s):  
B C Nephew ◽  
J Amico ◽  
H M Cai ◽  
A M Walker ◽  
R S Bridges
Keyword(s):  
Receptor Antagonist ◽  
Plasma Concentrations ◽  
Female Rats ◽  
Plasma Progesterone ◽  
Blood Samples ◽  
Period Effects ◽  
Preliminary Study ◽  
Nulliparous Female ◽  
Plasma Prl

The prolactin (PRL) receptor antagonist S179D PRL delays the onset of maternal behavior in steroid-primed nulliparous female rats. The present study investigated the role of the neural PRL system in the process of parturition. A preliminary study indicated that S179D PRL treatments administered by ALZET minipump to the lateral ventricle severely disrupted parturition. To examine the likely causes of this disruption, a group of timed-pregnant catheterized rats was continuously infused with S-179D PRL (0.001 and 0.1 ng/h) or vehicle control to the lateral ventricles for 3 days (gestation days 21–23), and serial blood samples were taken throughout this period. Effects of the treatments on parturition were recorded, and blood samples were assayed for PRL, progesterone, and oxytocin. Significantly fewer S179D PRL-treated rats successfully delivered by 1500 h on day 23 of gestation when compared with controls. The higher dose of S179D PRL also significantly suppressed the prepartum rise in PRL throughout the prepartum period, while the lower dose only affected plasma PRL during the first 24 h of treatment. No significant effects of the antagonist on plasma progesterone or oxytocin were detected. We conclude that disruption of parturition by S179D PRL is not caused by significant alterations in the plasma concentrations of progesterone or oxytocin. S179D PRL may indirectly act on parturition through the modulation of prepartum PRL. These findings suggest a previously unrecognized role for PRL in the regulation of parturition.

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.

PLASMA PROLACTIN AND PROGESTERONE RESPONSES TO MATING ARE ALTERED IN AGED RATS

1981 ◽  
Vol 90 (2) ◽  
pp. 179-191 ◽  
Author(s):  
S. HENDRICKS ◽  
C. A. BLAKE
Keyword(s):  
Plasma Concentrations ◽  
External Jugular Vein ◽  
Female Rats ◽  
Plasma Prolactin ◽  
Aged Rats ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Plasma Progesterone ◽  
The One ◽  
The Right

The effects of varying amounts of copulatory stimulation on patterns of plasma concentrations of prolactin and progesterone were evaluated in 3- and 12-month-old female rats. The 12-month-old group included rats which still exhibited oestrous cycles and rats in persistent vaginal oestrus (PVO). The extent of copulatory stimulation was defined by the number of intromissions received during mating: ≤5,15 or > 50. Blood samples were drawn over the 8 days after mating through a cannula inserted into the right external jugular vein. Plasma from the samples was assayed for prolactin and progesterone. In aged but still cyclic rats, pregnancy rates were positively correlated with the number of intromissions received during mating. Only one rat in PVO became pregnant. All animals which became pregnant and rats in PVO which, after mating, exhibited a disruption of the pattern of PVO, showed the nocturnal surge of plasma prolactin characteristic of pregnant and pseudopregnant rats. While these surges persisted until day 8 after mating in pregnant animals, they were absent by this time in the rats in PVO. Prolactin surges were present in some but not all of the aged rats which did not become pregnant. Progesterone concentrations were raised in all pregnant animals except the one pregnant rat in PVO and, while not related to the number of intromissions, concentrations were higher 8 days after mating in young compared with those in aged pregnant rats. Plasma progesterone was low in rats in PVO regardless of disruption of the pattern of PVO. We have concluded that the failure of limited copulatory stimulation to induce pregnancy in older rats results, at least in part, from its failure to initiate nocturnal prolactin surges. Nevertheless, our data suggest that matings which are not experimentally limited should provide ample stimulation to establish such surges. Although reduced plasma concentrations of prolactin and progesterone at pro-oestrus and reduced plasma progesterone through part of gestation may contribute to decreasing fertility in aged rats, other unidentified factors appear to be involved in mediating the capacity of extensive copulatory stimulation to induce pregnancy in these animals.

PLASMA CONCENTRATIONS OF PROLACTIN AND THYROTROPHIN DURING SUCKLING: EFFECTS OF STIMULATION OF THE MEDIAN EMINENCE

1978 ◽  
Vol 76 (3) ◽  
pp. 557-558 ◽  
Author(s):  
J. B. WAKERLEY ◽  
M. B. TER HAAR
Keyword(s):  
Direct Effect ◽  
Median Eminence ◽  
Plasma Concentrations ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Animal Physiology ◽  
Inhibiting Factor ◽  
Hypothalamic Level ◽  
Stimulation Of

A.R.C. Institute of Animal Physiology, Babraham, Cambridge, CB2 4AT (Received 1 November 1977) Thyrotrophin releasing hormone (TRH) can have a stimulatory effect on the release of both prolactin and thyrotrophin (TSH; Deis & Alonso, 1973), although in the rat, supraphysiological doses of TRH are required to affect the secretion of prolactin (Burnet & Wakerley, 1976). A more important factor in the control of the release of prolactin is considered to be prolactin release inhibiting factor (PIF), which is thought to act through the catecholamine, dopamine (MacLeod, 1976). Stimuli which cause the concomitant release of TSH and prolactin are thought to have a direct effect at the hypothalamic level such that neurones releasing TRH are excited, whereas those releasing PIF are inhibited. In the present work, we have tested this hypothesis using the suckling stimulus to elicit the simultaneous release of prolactin and TSH (Blake, 1974; Burnet & Wakerley, 1976). If

scholarly journals Epizootic Situation on Anaplasmosis of Small Ruminants in the Irkutsk Region

2021 ◽  
Vol 6 (1) ◽  
pp. 60-68
Author(s):  
O. V. Suntsova ◽  
V. A. Rar ◽  
O. V. Lisak ◽  
I. V. Meltsov ◽  
E. K. Doroschenko ◽  
...  
Keyword(s):  
Nucleotide Substitution ◽  
Small Ruminants ◽  
Wide Distribution ◽  
Anaplasma Ovis ◽  
Single Nucleotide ◽  
Blood Samples ◽  
Sheep Blood ◽  
Irkutsk Region ◽  
Probable Role

Anaplasmosis of ruminants is a group of natural focal infections caused by bacteria from the genus Anaplasma of the Anaplasmataceae family. The main etiological agent of anaplasmosis in sheep, goats, and wild ruminants is Anaplasma ovis, which parasitizes in the erythrocytes of these animals. The purpose of this study was the finding and identification of Anaplasma spp. in the blood of small ruminants using genetic methods and obtaining data on the distribution of anaplasmosis in the Irkutsk region. 20 goat blood samples, 611 sheep blood samples and 209 Dermacentor nuttalli ticks from 12 districts of the Irkutsk region were examined for the presence of Anaplasma spp. Only one type of anaplasma, A. ovis, was found among the genotyped samples. A. ovis was found in the blood of sheep and goats in all of the studied districts of the Irkutsk region. The proportion of sheep blood samples containing anaplasma DNA varied from 30 % to 85 %, in goats – from 10 % to 100 % in different districts, and averaged 57.8 % in sheep and 55,0 % in goats. Frequency of infection of D. nuttalli ticks with A. ovis was 5.7 %. The nucleotide sequences of the samples detected in the blood of small ruminants on the territory of the Irkutsk region differed from each other by a single nucleotide substitution and were identical to the sequences of the type strain Haibei, as well as the sequences of A. ovis previously found in the blood of sheep from Mongolia, deer from China, and Dermacentor niveus and Dermacentor nuttalli ticks from China. These sequences were also identical to the sequences previously found in the blood of sheep from Altai and in Dermacentor nuttalli ticks from Tuva, which indicates the wide distribution of these A. ovis genovariants in Siberia and the probable role of D. nuttalli as a carrier of the agent of anaplasmosis of small ruminants in the Irkutsk region.

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

Role of guanine nucleotide-binding proteins, Giα3 and Gsα, in dopamine and thyrotropin-releasing hormone signal transduction: evidence for competition and commonality

1996 ◽  
Vol 148 (3) ◽  
pp. 447-455 ◽  
Author(s):  
R D Kineman ◽  
T W Gettys ◽  
L S Frawley
Keyword(s):  
Signal Transduction ◽  
G Proteins ◽  
Cell Cultures ◽  
Intracellular Signaling ◽  
Receptor Activation ◽  
Pituitary Cell ◽  
Thyrotropin Releasing Hormone ◽  
Female Rats ◽  
Releasing Hormone

Abstract It is clear that dopamine (DA) at high concentrations (>100 nmol/l) inhibits the release of prolactin (PRL). Paradoxically, this monoamine at low concentrations (<10 nmol/l) has also been shown to augment PRL secretion. One possible explanation for these divergent effects is that DA binds receptors capable of interacting with multiple G protein subtypes that recruit opposing intracellular signaling pathways within lactotropes. To identify G proteins which couple DA receptor activation to PRL secretion, we have selectively immunoneutralized the activity of Giα3 and Gsα in primary cultures of rat pituitaries and subsequently tested the ability of these cultures to respond to high and low dose DA. Specifically, permeabilized pituitary cell cultures from random-cycling female rats were treated with control immunoglobulins (IgGs; 50 μg/ml) purified from preimmune serum (PII) or IgGs directed against the C-terminal portion of Giα3 or Gsα. After immunoneutralization of these G proteins, cells were challenged with 10 or 1000 nmol Da/l and the relative amount of PRL released was assessed by reverse hemolytic plaque assay. Results were expressed as % of basal values and compared. Under control conditions (PII), 1000 nmol DA/l inhibited (61·4 ±7·6% of basal values; mean ± s.e.m.) while 10 nmol DA/l augmented (120·0 ± 7·0%) PRL release in five separate experiments. Treatment of cells with anti-Giα3 attenuated the inhibitory effect of high dose DA (87·3 ± 14·5%). However, elimination of Giα3 activity did not significantly alter the PRL stimulatory effect of 10 nmol DA/l (121·0 ± 5·2%). Interestingly, immunoneutralization of Gsα resulted in a reciprocal shift in the activity of the lower dose of DA from stimulatory to inhibitory (69·7 ± 7·3%) while combined treatment of anti-Giα3 and anti-Gsα abrogated the responsiveness of pituitary cell cultures to either DA treatment (1000 nmol/l, 70·7 ± 12·5% and 10 nmol/l, 87·5 ± 21·4%). These data reveal that ligand-activated DA receptors can interact with both Giα3 and Gsα. Elimination of the stimulatory component (Gsα) favors the DA receptor activation of the inhibitory pathway (Giα3) suggesting a competition between negative and positive intracellular signaling mechanisms in normal lactotropes. In addition to DA treatment, we also challenged permeabilized pituitary cells with 100 nmol thyrotropin-releasing hormone (TRH)/1 as a positive control for secretory integrity. As anticipated, TRH stimulated PRL release to 188·0±31·0% of basal values under control conditions. Unexpectedly, immunoneutralization of Gsα completely blocked the ability of TRH to induce PRL release (101·8 ± 12·0% This neutralizing effect was specific to Gsα in that blockade of Giα3 activity had no significant effect on TRH-stimulated PRL release (166·2 ± 13·1%). These data are the first to support a direct role of Gsα in TRH signal transduction within PRL-secreting cells. Journal of Endocrinology (1996) 148, 447–455

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