Effects of constant infusion of gonadotrophin-releasing hormone in ovariectomized ewes with hypothalamo-pituitary disconnection: further evidence for differential control of LH and FSH secretion and the lack of a priming effect

1986 ◽  
Vol 111 (1) ◽  
pp. 43-49 ◽  
Author(s):  
I. J. Clarke ◽  
K. J. Burman ◽  
B. W. Doughton ◽  
J. T. Cummins
Keyword(s):  
Priming Effect ◽  
Physiological Saline ◽  
Constant Infusion ◽  
Releasing Hormone ◽  
Pulsatile Gnrh ◽  
Gonadotrophin Releasing Hormone ◽  
Rate Of Decline ◽  
Differential Control ◽  
Lh Secretion ◽  
Gnrh Infusion

ABSTRACT Experiments were conducted in ovariectomized ewes after hypothalamo-pituitary disconnection (HPD) (a) to examine LH and FSH secretion during constant infusion of gonadotrophin-releasing hormone (GnRH) or physiological saline and (b) to determine whether or not a constant GnRH background enhances or diminishes pituitary responsiveness to GnRH pulses. Whereas pulsatile GnRH infusions maintained LH and FSH secretion, constant infusions (125 or 250 ng/h) led to the complete cessation of LH secretion and reduced FSH secretion. The rate of decline of plasma FSH concentrations was significantly (P<0·01) greater in animals receiving 250 ng GnRH/h than in saline-treated animals, whereas that in animals receiving 125 ng/h was not significantly different. When GnRH pulses were administered during constant GnRH infusion, the plasma LH pulse amplitudes were similar to those seen without the GnRH background. These data show that, in ovariectomized-HPD ewes (a) FSH secretion does not require GnRH pulses and may merely reflect ongoing FSH synthesis and (b) a constant low background of GnRH does not affect pituitary responsiveness to GnRH pulses. J. Endocr. (1986) 111, 43–49

Relationship between gonadotrophin subunit gene expression, gonadotrophin-releasing hormone receptor content and pituitary and plasma gonadotrophin concentrations during the rebound release of FSH after treatment of ewes with bovine follicular fluid during the luteal phase of the cycle

1992 ◽  
Vol 8 (2) ◽  
pp. 109-118 ◽  
Author(s):  
J. Brooks ◽  
W. J. Crow ◽  
J. R. McNeilly ◽  
A. S. McNeilly
Keyword(s):  
Follicular Fluid ◽  
Luteal Phase ◽  
Gnrh Receptor ◽  
Mrna Levels ◽  
Α Subunit ◽  
Luteal Regression ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Cessation Of Treatment

ABSTRACT The modulation of FSH secretion at the beginning and middle of the follicular phase of the cycle represents the key event in the growth and selection of the preovulatory follicle. However, the mechanisms that operate within the pituitary gland to control the increased release of FSH and its subsequent inhibition in vivo remain unclear. Treatment of ewes with bovine follicular fluid (bFF) during the luteal phase has been previously shown to suppress the plasma concentrations of FSH and, following cessation of treatment on day 11, a rebound release of FSH occurs on days 12 and 13. When luteal regression is induced on day 12, this hypersecretion of FSH results in an increase in follicle growth and ovulation rate. To investigate the mechanisms involved in the control of FSH secretion, ewes were treated with twice daily s.c. injections of 5 ml bFF on days 3–11 of the oestrous cycle and luteal regression was induced on day 12 with prostaglandin (PG). The treated ewes and their controls were then killed on day 11 (luteal), or 16 or 32h after PG and their pituitaries removed and halved. One half was analysed for gonadotrophin and gonadotrophin-releasing hormone (GnRH) receptor content. Total pituitary RNA was extracted from the other half and subjected to Northern analysis using probes for FSH-β, LH-β and common α subunit. Frequent blood samples were taken and assayed for gonadotrophins. FSH secretion was significantly (P<0.01) reduced during bFF treatment throughout the luteal phase and then significantly (P<0.01) increased after cessation of treatment, with maximum secretion being reached 18– 22h after PG, and then declining towards control values by 32h after PG. A similar pattern of LH secretion was seen after bFF treatment. Pituitary FSH content was significantly (P<0.05) reduced by bFF treatment at all stages of the cycle. No difference in the pituitary LH content was seen. The increase in GnRH receptor content after PG in the controls was delayed in the treated animals. Analysis of pituitary mRNA levels revealed that bFF treatment significantly (P<0.01) reduced FSH-β mRNA levels in the luteal phase. Increased levels of FSH-β, LH-β and α subunit mRNA were seen 16h after PG in the bFF-treated animals, at the time when FSH and LH secretion from the pituitary was near maximum. These results suggest that the rebound release of FSH after treatment with bFF (as a source of inhibin) is related to a rapid increase in FSH-β mRNA, supporting the concept that the rate of FSH release is directly related to the rate of synthesis.

Effects of corticotropin-releasing hormone and its antagonist on the gene expression of gonadotrophin-releasing hormone (GnRH) and GnRH receptor in the hypothalamus and anterior pituitary gland of follicular phase ewes

2011 ◽  
Vol 23 (6) ◽  
pp. 780 ◽  
Author(s):  
Magdalena Ciechanowska ◽  
Magdalena Łapot ◽  
Tadeusz Malewski ◽  
Krystyna Mateusiak ◽  
Tomasz Misztal ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Follicular Phase ◽  
Gnrh Receptor ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Crh Receptors

There is no information in the literature regarding the effect of corticotropin-releasing hormone (CRH) on genes encoding gonadotrophin-releasing hormone (GnRH) and the GnRH receptor (GnRHR) in the hypothalamus or on GnRHR gene expression in the pituitary gland in vivo. Thus, the aim of the present study was to investigate, in follicular phase ewes, the effects of prolonged, intermittent infusion of small doses of CRH or its antagonist (α-helical CRH 9-41; CRH-A) into the third cerebral ventricle on GnRH mRNA and GnRHR mRNA levels in the hypothalamo–pituitary unit and on LH secretion. Stimulation or inhibition of CRH receptors significantly decreased or increased GnRH gene expression in the hypothalamus, respectively, and led to different responses in GnRHR gene expression in discrete hypothalamic areas. For example, CRH increased GnRHR gene expression in the preoptic area, but decreased it in the hypothalamus/stalk median eminence and in the anterior pituitary gland. In addition, CRH decreased LH secretion. Blockade of CRH receptors had the opposite effect on GnRHR gene expression. The results suggest that activation of CRH receptors in the hypothalamus of follicular phase ewes can modulate the biosynthesis and release of GnRH through complex changes in the expression of GnRH and GnRHR genes in the hypothalamo–anterior pituitary unit.

Induction of luteinized unruptured follicles in the rat after injection of luteinizing hormone early in pro-oestrus

1995 ◽  
Vol 132 (1) ◽  
pp. 91-96 ◽  
Author(s):  
John AM Mattheij ◽  
Hans JM Swarts
Keyword(s):  
Luteinizing Hormone ◽  
The Netherlands ◽  
Small Dose ◽  
Great Majority ◽  
Gnrh Analogue ◽  
Releasing Hormone ◽  
Animal Physiology ◽  
Cause Of Formation ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Mattheij JAM, Swarts HJM. Induction of luteinized unruptured follicles in the rat after injection of luteinizing hormone early in pro-oestrus. Eur J Endocrinol 1995;132:91–6. ISSN 0804–4643 The cause of formation of luteinized unruptured follicles (LUF) is unknown. Formation of LUF was studied after injection of a varying small dose of luteinizing hormone (LH) with or without subsequent injection of gonadotrophin-releasing hormone (GnRH); in addition, the effect of suppression of prolactin on LUF formation was studied. Luteinization without ovulation occurred in virtually all graafian follicles, if 0.5–1.0 μg of LH was injected some hours before the presumed endogenous LH surge (suppressed by Nembutal); with increasing doses of LH progressively increasing numbers of ovulations were observed. If in early pro-oestrus 1 μg of GnRH was given 4 h after 1 μg of LH, formation of LUF was partly prevented; if the interval between LH and GnRH was 8 h or more, the great majority of graafian follicles developed into LUF. If early in pro-oestrus 1 μg of LH was given and 8 h later 0.1 μg of a potent GnRH analogue, about 50% of the follicles became LUF; in similarly treated rats, suppression of prolactin by ergocryptine reduced but did not prevent LUF formation. The data support the idea that deficient LH secretion in the period before ovulation may be involved in the formation of LUF. John AM Mattheij, Department of Human and Animal Physiology, Haarweg 10, 6709 PJ Wageningen, The Netherlands

Infantile ovariectomy potentiates the stimulatory effect of oestrogen/progesterone on LH secretion in the rat

1985 ◽  
Vol 106 (1) ◽  
pp. 133-139 ◽  
Author(s):  
M. Wilkinson ◽  
R. Bhanot
Keyword(s):  
Inhibitory Mechanism ◽  
Releasing Hormone ◽  
Oestradiol Benzoate ◽  
Gonadotrophin Releasing Hormone ◽  
Prepubertal Rats ◽  
Lh Secretion

ABSTRACT Ovariectomy of prepubertal rats (9 days of age) eliminates the ability of the opiate peptide FK 33-824 to inhibit LH secretion when tested 19 days later. We have investigated whether this removal of opiate inhibition would modify the LH/FSH response to stimulation with oestradiol benzoate/progesterone priming. Ovariectomy of rats during infancy (9 days after birth) amplifies the stimulatory effects of these steroids on LH/FSH secretion when tested 19 days later. This amplification was not seen in rats ovariectomized before (day 24) or after puberty (day 43) and tested 19 days later. The pituitary content of LH/FSH does not appear to contribute to this phenomenon, though increased responsiveness to injected gonadotrophin-releasing hormone (GnRH) is clearly involved; ovariectomy at day 9 is considerably more effective than ovariectomy at day 24 of life in enhancing the response to GnRH. We conclude that infantile ovariectomy either removes, or prevents the development of, a hypothalamic inhibitory mechanism which normally modulates the responsiveness of the pituitary to stimulation with GnRH. J. Endocr. (1985) 106, 133–139

Gonadotrophin-releasing hormone (GnRH) overcomes GnRH antagonist-induced suppression of LH secretion in primates

1986 ◽  
Vol 110 (1) ◽  
pp. 145-150 ◽  
Author(s):  
G. R. Marshall ◽  
F. Bint Akhtar ◽  
G. F. Weinbauer ◽  
E. Nieschlag
Keyword(s):  
Gnrh Antagonist ◽  
Receptor Occupancy ◽  
Gnrh Receptor ◽  
Dependent Manner ◽  
Response Curves ◽  
Gnrh Antagonists ◽  
Releasing Hormone ◽  
Gonadotrophin Secretion ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

ABSTRACT If the suppressive effects of gonadotrophin-releasing hormone (GnRH) antagonists on gonadotrophin secretion are mediated through GnRH-receptor occupancy alone, it should be possible to restore serum gonadotrophin levels by displacing the antagonist with exogenous GnRH. To test this hypothesis, eight adult crab-eating macaques (Macaca fascicularis), weight 4·7–7·6 kg, were subjected to the following treatment regimens. A GnRH-stimulation test was performed before and 4, 12 and 24 h after a single s.c. injection of the GnRH antagonist (N-Ac-d-p-Cl-Phe1,2,d-Trp3,d-Arg6,d-Ala10)-GnRH (ORG 30276). The stimulation tests were performed with 0·5, 5·0 or 50 μg GnRH given as a single i.v. bolus. Blood was taken before and 15, 30 and 60 min after each bolus for analysis of bioactive LH and testosterone. The GnRH-challenging doses were given as follows: 0·5 μg GnRH was injected at 0 and 4 h, followed by 5·0 μg after 12 h and 50 μg after 24 h. One week later, 5·0 μg GnRH were given at 0 and 4 h, followed by 50 μg after 12 h and 0·5 μg after 24 h. Finally, after another week, the GnRH challenges began with 50 μg at 0 and 4 h, followed by 0·5 μg at 12 h and 5·0 μg at 24 h. This design permitted comparison of the LH and testosterone responses with respect to the dose of GnRH and the time after administration of GnRH antagonist. The areas under the response curves were measured and statistical evaluation was carried out by means of non-parametric two-way analysis of variance followed by the multiple comparisons of Wilcoxon and Wilcox. Four hours after the antagonist was injected, the LH and testosterone responses to all three doses of GnRH were suppressed. At the lowest dose of GnRH (0·5 μg) the responses remained reduced even after 24 h, whereas the higher doses of GnRH elicited an LH and testosterone response at 12 and 24 h which was not significantly different from that at 0 h. These data demonstrate that the suppression of LH secretion by a GnRH antagonist in vivo can be overcome by exogenously administered GnRH in a dose- and time-dependent manner, thus strongly supporting the contention that GnRH antagonists prevent gonadotrophin secretion by GnRH-receptor occupancy. J. Endocr. (1986) 110, 145–150

Effects of a preovulatory administered depot gonadotrophin-releasing hormone agonist on reproductive hormone levels and pregnancy outcome in gilts

2006 ◽  
Vol 18 (8) ◽  
pp. 857 ◽  
Author(s):  
F. Schneider ◽  
K.-P. Brüssow
Keyword(s):  
Pregnancy Outcome ◽  
Control Group ◽  
Luteal Function ◽  
Releasing Hormone ◽  
Estrone Sulfate ◽  
Endocrine Parameters ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Mean Concentration ◽  
Implantation Period

The present study aimed to explore the influence of a preovulatory administered depot gonadotrophin-releasing hormone (GnRH) agonist (GnRHa; Decapeptyl®Depot) on the endocrine parameters and pregnancy outcome of gilts (n = 6). A GnRHa-supported preovulatory luteinising hormone (LH) surge was detected in all treated gilts. LH pulses were abolished completely by depot GnRHa on Day 7 and partly on Day 21 of pregnancy. In this treatment group (n = 6) four gilts were pregnant at slaughter on Day 28. In the control group receiving Gonavet®, a non-formulated GnRHa (n = 6), all pigs showed LH pulses and were pregnant at slaughter on Day 28 of gestation. Mean progesterone concentrations were elevated in controls during the early luteal phase and were similar for both groups during the implantation period. Mean concentration of unoccupied progesterone receptor was significantly higher in uterine myometrium than in endometrium, but without treatment effects. Peripheral estrone sulfate concentrations showed a similar increase in all pregnant gilts on Days 17 and 18, and remained elevated. In summary, treatment with a depot GnRHa for synchronisation of ovulation alters pulsatile LH secretion during early pregnancy in pigs. In general, this alteration seems not to exert an injurious influence on luteal function and, therefore, on embryo and early fetal development.

Secretion rates and short-term patterns of gonadotrophin-releasing hormone, FSH and LH in the normal stallion in the breeding season

1988 ◽  
Vol 117 (2) ◽  
pp. 197-206 ◽  
Author(s):  
C. H. G. Irvine ◽  
S. L. Alexander
Keyword(s):  
Breeding Season ◽  
Venous Blood ◽  
Pulse Amplitude ◽  
Interpulse Interval ◽  
Statistical Testing ◽  
Pulse Interval ◽  
Apparent Difference ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

ABSTRACT Pituitary venous blood was collected by a painless non-surgical cannulation method from five ambulatory stallions at 5-min intervals for 5–6 h during the breeding season. In four adult stallions, statistical analysis showed that pulses of gonadotrophin-releasing hormone (GnRH) and LH were coincident (P <0·01), as were pulses of FSH and LH (P <0·05). Furthermore, the patterns of changes in concentration of FSH and LH were highly correlated in each of the four stallions. However, seemingly ineffective pulses of GnRH were also observed, with 28% of GnRH pulses failing to induce a significant gonadotrophin pulse. In the four adult stallions the amplitude of pituitary venous gonadotrophin pulses varied markedly but no correlation with GnRH pulse amplitude was observed. Peak secretion of FSH, but not LH, during pulses was correlated with the length of the interpulse interval. Consequently, the ratio of FSH to LH during peaks was least (P <0·02) when the interpulse interval was 30 min or less. Thus, differential FSH and LH secretion was achieved within a constant steroid milieu. Two stallions had regular contact with oestrous mares, and in these horses the secretion of GnRH and gonadotrophins occurred almost continuously with rapid, rhythmic pulses superimposed upon a tonic background. Mean (± s.d.) interval between GnRH pulses was 31·4 ± 9·8 min and 27·7 ± 10·1 min. This secretory pattern was not observed in the two stallions which had infrequent contact with oestrous mares, although the small numbers precluded statistical testing of this apparent difference. No GnRH pulses were observed in one of these stallions, while in the other mean (± s.d.) GnRH pulse interval was 45·0 ± 48·7 min, the large variance being partly due to rapid pulses during a period in which the stallion teased mares. The fifth stallion was pubertal, and GnRH and LH secretion occurred in 15 and 0% of samples respectively, while low levels of FSH secretion were observed in 37% of samples and jugular testosterone levels were immeasurably low. We conclude that there is a statistically significant synchrony between pulses of GnRH, LH and FSH in the pituitary venous blood of stallions. Furthermore, decreasing intervals between gonadotrophin pulses result in a significant reduction in secretion of FSH but not LH. J. Endocr. (1988) 117, 197–206

Exogenous gonadotrophin-releasing hormone (GnRH) stimulates LH secretion in male monkeys (Macaca fascicularis) treated chronically with high doses of a GnRH antagonist

1992 ◽  
Vol 133 (3) ◽  
pp. 439-445 ◽  
Author(s):  
G. F. Weinbauer ◽  
P. Hankel ◽  
E. Nieschlag
Keyword(s):  
Gnrh Antagonist ◽  
Prolonged Exposure ◽  
Receptor Occupancy ◽  
Gnrh Receptor ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Testosterone Secretion ◽  
Stimulation Tests ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

ABSTRACT We reported previously that after a single injection of a gonadotrophin-releasing hormone (GnRH) antagonist to male monkeys, exogenous GnRH stimulated LH secretion in a time- and dose-dependent manner, indicating that GnRH antagonist-induced blockade of LH secretion resulted from pituitary GnRH receptor occupancy. The present study was performed to investigate whether GnRH can also restore a blockade of LH and testosterone secretion during chronic GnRH antagonist administration. Four adult male cynomolgus monkeys (Macacafascicularis) received daily s.c. injections of the GnRH antagonist [N-Ac-d-pCl-Phe1,2,d-TRP3,d-Arg6,d-Ala10]-GnRH (ORG 30276) at a dose of 1400–1600 μg/kg for 8 weeks. Before the GnRH antagonist was given and during weeks 3 and 8 of treatment, pituitary stimulation tests were performed with 0·5, 5, 50 and 500 μg synthetic GnRH, administered in increasing order at intervals of 24 h. At 8 weeks, a dose of 1000 μg GnRH was also given. All doses of GnRH significantly (P < 0·05) stimulated serum concentrations of bioactive LH (3- to 8-fold) and testosterone (2·6- to 3·8-fold) before the initiation of GnRH antagonist treatment. After 3 weeks of GnRH antagonist treatment, only 50 and 500 μg GnRH doses were able to increase LH and testosterone secretion. Release of LH was significantly (P < 0·05) more elevated with 500 μg compared with 50 μg GnRH. After 8 weeks, only the highest dose of 1000 μg elicited a significant (P < 0·05) rise in LH secretion. Basal hormone levels just before the bolus injection of GnRH were similar (P > 0·10–0·80). This finding eliminated the possibility that the increasing doses of GnRH had primed the pituitary thereby resulting in higher stimulatory effects of the larger doses of GnRH. In conclusion, the present data indicate that, even after prolonged exposure to a GnRH antagonist, the pituitary retains some degree of responsiveness to GnRH. This observation supports the view that the inhibitory effects of chronic GnRH antagonist treatment are also mediated, at least in part, by occupancy of the pituitary GnRH receptor rather than by receptor down-regulation. Journal of Endocrinology (1992) 133, 439–445

Lipopolysaccharide reduces gonadotrophin-releasing hormone (GnRH) gene expression: role of RFamide-related peptide-3 and kisspeptin

2019 ◽  
Vol 31 (6) ◽  
pp. 1134 ◽  
Author(s):  
Chooi Yeng Lee ◽  
ShengYun Li ◽  
Xiao Feng Li ◽  
Daniel A. E. Stalker ◽  
Claire Cooke ◽  
...  
Keyword(s):  
Gene Expression ◽  
In Situ Hybridisation ◽  
Releasing Hormone ◽  
Related Peptide ◽  
Concomitant Reduction ◽  
Intracerebroventricular Injections ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

RFamide-related peptide (RFRP)-3 reduces luteinising hormone (LH) secretion in rodents. Stress has been shown to upregulate the expression of the RFRP gene (Rfrp) with a concomitant reduction in LH secretion, but an effect on expression of the gonadotrophin-releasing hormone (GnRH) gene (Gnrh1) has not been shown. We hypothesised that lipopolysaccharide (LPS)-induced stress affects expression of Rfrp, the gene for kisspeptin (Kiss1) and/or Gnrh1, leading to suppression of LH levels in rats. Intracerebroventricular injections of RFRP-3 (0.1, 1, 5 nmol) or i.v. LPS (15μgkg−1) reduced LH levels. Doses of 1 and 5 nmol RFRP-3 were then administered to analyse gene expression by in situ hybridisation. RFRP-3 (5 nmol) had no effect on Gnrh1 or Kiss1 expression. LPS stress reduced GnRH and Kiss1 expression, without affecting Rfrp1 expression. These data indicate that LPS stress directly or indirectly reduces Gnrh1 expression, but this is unlikely to be due to a change in Rfrp1 expression.

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