FSH causes a time-dependent stimulation of preovulatory follicle growth in the absence of pulsatile LH secretion in ewes chronically treated with gonadotrophin-releasing hormone agonist

1990 ◽  
Vol 126 (2) ◽  
pp. 297-307 ◽  
Author(s):  
H. M. Picton ◽  
C. G. Tsonis ◽  
A. S. McNeilly
Keyword(s):  
Plasma Concentration ◽  
Gnrh Agonist ◽  
Corpora Lutea ◽  
Preovulatory Follicle ◽  
Follicle Growth ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
The Mean ◽  
Stimulation Of

ABSTRACT The study investigated the relationship between the plasma concentration of FSH and the stimulation of preovulatory follicle growth in vivo in ewes chronically treated with the gonadotrophin-releasing hormone (GnRH) agonist buserelin (HOE 766). Welsh Mountain ewes with regular oestrous cycles were treated for 6 weeks with two discs implants placed s.c., each containing 5 mg of the agonist in a matrix of polyhydroxybutyric acid. Treatment with the agonist for 35 days produced a sustained suppression of the plasma concentration of FSH, stopped the pulsatile release of LH and prevented follicular development beyond 2·5 mm diameter. There was no difference between the total number of follicles > 1·0 mm diameter present in the ovaries of GnRH agonist-treated ewes and day 8 luteal phase control ewes. During the sixth week of agonist treatment ewes were infused with ovine FSH (6 μg NIADDK-oFSH16/h) in the presence of only basal concentrations of LH. After 24, 48, 72 or 120 h of FSH infusion, the mean number of follicles > 1 ·0 mm diameter per ewe was not significantly different between treated and control animals. Infusion of FSH caused a timedependent increase in (1) the number of follicles per ovary >2·5 mm, (2) the mean diameter of these follicles and (3) the proportion of the large follicles which could be classified as oestrogenic (> 3·7 nmol oestradiol/follicle per h in vitro). Injection of human chorionic gonadotrophin (750IU i.m.) after 120 h of FSH infusion caused the majority of these large follicles to ovulate and form apparently normal corpora lutea. These results indicate that, in the absence of pulsatile LH, FSH stimulates the growth of normal large oestrogenic follicles which, when stimulated, ovulate to produce viable corpora lutea. Journal of Endocrinology (1990) 126, 297–307

A gonadotrophin-releasing hormone (GnRH) antagonist inhibits GnRH- but not LH-induced meiosis in follicle-enclosed rat oocytes in vitro

1982 ◽  
Vol 101 (2) ◽  
pp. 264-267 ◽  
Author(s):  
C. Ekholm ◽  
T. Hillensjö ◽  
W. J. Le Maire ◽  
C. Magnusson ◽  
C. S. Sheela Rani
Keyword(s):  
Gnrh Agonist ◽  
Gnrh Antagonist ◽  
Similar Response ◽  
Releasing Hormone ◽  
Lactate Accumulation ◽  
Receptor Sites ◽  
Gonadotrophin Releasing Hormone ◽  
Stimulation Of

Abstract. Previous studies have shown that gonadotrophin-releasing hormone (GnRH) can induce resumption of meiosis in follicle-enclosed rat oocytes. In the present study a GnRH antagonistic analogue ([d-pGlul, d-Phe2,-d-Trp3,6]LRF) was found to effectively abolish the stimulatory effect of a GnRH agonist upon resumption of meiosis and lactate accumulation in isolated pre-ovulatory rat follicles but the have no effect on LH stimulation of these parameters. It is concluded that although LH and GnRH can evoke a similar response they act through separate receptor sites and that it is unlikely that GnRH mediates the effect of LH on meiosis or glycolysis.

The antagonistic effect of exogenous LH pulses on FSH-stimulated preovulatory follicle growth in ewes chronically treated with a gonadotrophin-releasing hormone agonist

1990 ◽  
Vol 127 (2) ◽  
pp. 273-283 ◽  
Author(s):  
H. M. Picton ◽  
C. G. Tsonis ◽  
A. S. McNeilly
Keyword(s):  
Luteal Phase ◽  
Follicular Development ◽  
High Amplitude ◽  
Follicle Growth ◽  
High Concentration ◽  
Continuous Administration ◽  
Releasing Hormone ◽  
Low Concentrations ◽  
Gonadotrophin Releasing Hormone ◽  
The Mean

ABSTRACT The hypogonadotrophism model induced by the chronic administration of gonadotrophin-releasing hormone (GnRH) agonist was used to investigate the effects of different concentrations of FSH with or without LH pulses on the stimulation of follicular development in the ewe. Continuous administration of an agonist (buserelin) by osmotic minipump to thirty-six Welsh Mountain ewes from the early luteal phase for 5 weeks resulted in a sustained suppression of the plasma concentration of FSH and inhibited the pulsatile release of LH. The inhibition of gonadotrophin secretion was due to the desensitization and/or down-regulation of pituitary gonadotroph function, since the agonist-treated animals showed no response to a challenge of 1 μg GnRH. During week 6 of agonist treatment, ewes were infused with either 4-hourly pulses of ovine LH (9 μg/pulse), low concentrations of ovine FSH (3 μg/h) or high concentrations of FSH (9 μg/h) alone or with 4-hourly pulses of LH. After 5 days of gonadotrophin infusion, there was no difference between the mean number of follicles per ewe from the animals treated with LH alone, low concentrations of FSH with or without LH pulses or the high concentration of FSH alone compared with the mean number of follicles from control ewes on day 8 of the luteal phase. Infusion of the high concentration of FSH alone stimulated the development of an increased number of large oestrogenic follicles (follicles > 2·5 mm in diameter and secreting > 3·7 nmol oestradiol/h in vitro) compared with control ewes. The addition of high-amplitude LH pulses to the infusion of the high concentration of FSH prevented follicles developing beyond 2·5 mm in diameter, but doubled the number of small follicles (≤2·5 mm) present in the ovaries. These results show that normal follicular development can be induced by physiological concentrations of FSH alone in the absence of pulsatile LH release. The addition of high-amplitude LH pulses antagonized this stimulatory effect of FSH on follicle growth in the ewe. Journal of Endocrinology (1990) 127, 273–283

Effect of basal and pulsatile LH release on FSH-stimulated follicle growth in ewes chronically treated with gonadotrophin-releasing hormone agonist

1991 ◽  
Vol 128 (3) ◽  
pp. 449-456 ◽  
Author(s):  
H. M. Picton ◽  
A. S. McNeilly
Keyword(s):  
Gnrh Agonist ◽  
Follicular Development ◽  
Follicle Growth ◽  
Releasing Hormone ◽  
Normal Number ◽  
Stage Of Development ◽  
Normal Diameter ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Follicular Response

ABSTRACT Ewes chronically treated with gonadotrophin-releasing hormone (GnRH) agonist were used to investigate the importance of the peripheral concentration of LH in FSH-stimulated follicular development. Twenty-four Welsh Mountain ewes were treated with two agonist implants containing 3·3 mg buserelin. During week 6 of treatment all the ewes were given a 72-h continuous infusion of ovine FSH alone (3 μg/h) or FSH with large (7·5 μg)- or small (2·5 μg) amplitude pulses of ovine LH delivered at 4-hourly intervals. The importance of baseline LH throughout the FSH infusion was evaluated in six animals which were treated with a specific antiserum against bovine LH (LH-AS) 15–20 h before the start of FSH treatment. In the absence of LH-AS, infusion of FSH alone or with large or small pulses of LH stimulated the development of a normal number of small follicles (≤ 2·5 mm in diameter) and large follicles (> 2·5 mm in diameter). These follicles had normal diameter and steroid secretion compared with control ewes on day 8 of the luteal phase. In contrast, the animals pretreated with LH-AS developed no follicles > 2·0 mm in diameter but the number of small follicles per ewe was significantly (P < 0·05) increased. These results support the hypothesis that FSH in the absence of pulsatile LH release stimulates preovulatory follicular development in ewes treated with GnRH agonist. The follicular response to LH pulses of different amplitude is dependent on both the stage of development of the follicle and the peripheral concentration of FSH. The endogenous basal level of LH present throughout the FSH infusion is essential for FSH to induce follicle growth beyond > 2·5 mm in diameter. Journal of Endocrinology (1991) 128, 449–456

THE EFFECTS OF TESTOSTERONE AND ITS 5α-REDUCED METABOLITES ON PITUITARY RESPONSIVENESS TO GONADOTROPHIN-RELEASING HORMONE (Gn-RH)

1977 ◽  
Vol 86 (4) ◽  
pp. 728-732 ◽  
Author(s):  
Y. Epstein ◽  
B. Lunenfeld ◽  
Z. Kraiem
Keyword(s):  
Pituitary Gland ◽  
Mature Male ◽  
Male Rats ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Low Levels ◽  
High Doses ◽  
Dose Dependent ◽  
Stimulation Of

ABSTRACT The aim of this study was to investigate effects of androgens on gonadotrophin release in response to gonadotrophin-releasing hormone (Gn-RH) stimulation in vitro. Hemipituitaries of mature male rats were pre-incubated for 90 min with T, DHT, 3α- or 3β-diol (4 ng or 4 μg/ml medium), and the incubation continued for 240 min after adding Gn-RH (1 ng/ml medium). Gn-RH caused a 4-5-fold rise in the secretion of LH and a 2-fold rise in FSH secretion. The effect of the androgens was dose-dependent. At low levels, T and DHT exerted no effect on Gn-RH-stimulated gonadotrophin release, whereas the two androstanediols (3α- and 3β-diol) augmented the Gn-RH stimulation of both gonadotrophins, though preferentially LH. With high doses of androgens, the results obtained showed: a) no effect of T; b) DHT suppression of the Gn-RH-stimulated FSH release; c) suppression of Gn-RH stimulation by 3α- and 3β-diol regarding both LH and FSH. It is concluded that T exerts through its reduced metabolites a feedback effect on the pituitary gland responsiveness to Gn-RH stimulation.

Long-term effects of a gonadotrophin-releasing hormone agonist ([d-Ser(But)6]GnRH(1–9)nonapeptide-ethylamide) on gonadotrophin secretion from human pituitary gonadotroph cell adenomas in vitro

1988 ◽  
Vol 118 (3) ◽  
pp. 491-496 ◽  
Author(s):  
M. Daniels ◽  
P. Newland ◽  
J. Dunn ◽  
P. Kendall-Taylor ◽  
M. C. White
Keyword(s):  
Gnrh Agonist ◽  
In Vitro Release ◽  
Long Term Effects ◽  
Human Pituitary ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Gonadotrophin Secretion ◽  
Gonadotrophin Releasing Hormone

ABSTRACT We have studied the effects of TRH and native gonadotrophin-releasing hormone (GnRH), and of a GnRH agonist (Buserelin; [d-Ser(But)6]GnRH(1–9) nonapeptide-ethylamide), on LH, FSH, α subunit and LH-β subunit secretion from three human gonadotrophin-secreting pituitary adenomas in dispersed cell culture. During a 24 h study, treatment with 276 nmol TRH/1 resulted in a significant (P < 0·05) stimulated release of FSH and α subunit from all three adenomas, and LH from the two adenomas secreting detectable concentrations of this glycoprotein; treatment with 85 nmol GnRH/l significantly (P < 0·05) stimulated the release of α subunit from all three, but FSH from only two and LH from only one adenoma. During a long-term 28-day study, basal FSH and α subunit concentrations were maintained, but secretion of LH, and LH-β (detectable from one tumour only), declined with time from two of the three adenomas. Addition of Buserelin to the cultures resulted in the continuous (P < 0·05) stimulation of α subunit secretion from all three adenomas, and of LH and FSH from two, whilst a transient stimulatory effect on LH and FSH secretion was seen from a third adenoma, with subsequent secretion rates declining towards control values. These data show that human gonadotrophin-secreting adenomas demonstrate variable stimulatory responses to hypothalamic TRH and GnRH, and that during chronic treatment with a GnRH agonist the anticipated desensitizing effect of the drug was not observed in two out of three adenomas studied. The mechanism for this is not clear, but such drugs are unlikely to be of therapeutic value in the management of gonadotrophin-secreting tumours. The data also suggest that GnRH and GnRH agonists have a differential effect on the in-vitro release of intact gonadotrophins and the common α subunit. J. Endocr. (1988) 118, 491–496

83 Response to follicle-stimulating hormone superstimulation in heifers with ovarian activity suppressed by active immunization against gonadotrophin-releasing hormone

2021 ◽  
Vol 33 (2) ◽  
pp. 149
Author(s):  
N. E. S. Pereira ◽  
L. P. Martins ◽  
R. M. Moura ◽  
L. R. O. Dias ◽  
M. A. S. Peixer ◽  
...  
Keyword(s):  
Active Immunization ◽  
Repeated Measure ◽  
Ovarian Activity ◽  
Corpora Lutea ◽  
Follicle Growth ◽  
Releasing Hormone ◽  
Significant Difference ◽  
Follicle Size ◽  
Gonadotrophin Releasing Hormone ◽  
Group B

In the present study, we evaluated the ovarian response to exogenous FSH stimulation in the absence of endogenous LH, using as experimental model heifers immunized against GnRH. Pubertal, cycling Nelore (Bos indicus) heifers were allocated into three experimental groups: (1) non-immunized, FSH stimulated (B−FSH+, n=5), (2) immunized, FSH stimulated (B+FSH+, n=5), and (3) immunized, nonstimulated (B+FSH−, n=5). Active immunization was obtained by 3 subcutaneous injections of 1.0mL anti-gonadotrophin-releasing hormone vaccine (Bopriva, Zoetis), given at 20-day intervals. Effective immunization was characterised by the absence of growing follicles &gt;4mm or corpora lutea (CL) on the ovaries. Follicular wave emergence was synchronized in groups B+FSH+ and B+FSH− by follicle ablation, and in group B−FSH+ by using of a protocol consisting of an injection of 2mg of oestradiol benzoate and 0.5mg of sodium cloprostenol, and insertion of an intravaginal progesterone (P4) device (1g). Four days later (Day 0), groups B−FSH+ and B+FSH+ received 100mg of NIH-FSH-P1 (Folltropin-V, Vetoquinol), injected twice-a-day in 8 decreasing doses, and group B+FSH− received saline. Transvaginal ultrasonography (7.5MHz) was performed daily from Days 0 to 4 and the number and size of follicles were recorded. P4 devices of group B-FSH+ were removed at Day 3. All heifers underwent ovum pickup (OPU) at Day 4, and the cumulus–oocyte complexes (COC) recovered were graded for quality. Viable COC were used for invitro embryo production. The heifers were re-evaluated at Day 11 (7 days after OPU). The GLIMMIX procedure from SAS (SAS Institute Inc.) with repeated-measure statement was used to analyse the effects of group, day, and interactions; and the Chi-squared method was used to analyse binomial data. The results are shown as mean±s.e.m. A progressive increase in average follicle size was observed in groups B−FSH+ and B+FSH+ (P&lt;0.0001), whereas no follicle growth was observed in group B+FSH− (P&gt;0.05). Follicle growth rate was similar between groups B−FSH+ and B+FSH+, and both were greater than group B+FSH− (1.2±0.2 and 1.1±0.1 vs. 0.0±0.1 mm/d; P&lt;0.0001). However, the smaller follicle size in group B+FSH+ at Day 0 resulted in smaller follicle size at Day 4, compared with group B−FSH+ (2.4±0.1 vs. 3.6±0.2 and 6.9±0.7 vs. 8.2±0.6mm, respectively; P&lt;0.05). There was no (P&gt;0.05) difference in the number of COC recovered among groups. The group B+FSH+ yielded fewer (P&lt;0.01) COC of grades I and II and more (P&lt;0.01) degenerated oocytes than groups B−FSH+ and B+FSH− (41.2% vs. 80.0% and 68.0%, and 34.0% vs. 19.8 and 7.0%, respectively). Nevertheless, blastocyst rates were similar (P&gt;0.05) for B−FSH+, B+FSH+, and B+FSH− (57.1%, 45.9% and 44.2%, respectively). Residual follicles or luteal tissue were observed after OPU only in group B−FSH+, resulting in a significant difference in the size of ovaries between Days 0 and 11, compared with that of groups B+FSH+ and B+FSH− (3.7±1.4 vs. 0.2±0.2 and −0.2±0.2cm2, respectively; P&lt;0.05). In summary, exogenous FSH supported follicle growth but did not improve oocyte quality in heifers immunized against GnRH. This research was funded by CAPES.

Effect of chronic exposure to a gonadotrophin-releasing hormone agonist on in vitro responsiveness of ovine pituitary cells to inhibin, activin and oestradiol

1994 ◽  
Vol 140 (3) ◽  
pp. 483-493 ◽  
Author(s):  
S Muttukrishna ◽  
P G Knight
Keyword(s):  
Gnrh Agonist ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Cell Content ◽  
Releasing Hormone ◽  
Basal Release ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

Abstract To investigate the extent to which the direct actions of inhibin, activin and oestradiol on pituitary output of FSH and LH are dependent on the presence of functional gonadotrophin-releasing hormone (GnRH) receptors, we have compared the effects of these agents on cultured ovine pituitary cells derived from control and GnRH agonist-suppressed ewes. Chronic treatment with GnRH agonist reduced plasma LH and FSH levels (P<0·01) and abolished GnRH-induced release of LH and FSH both in vivo and in vitro. As expected, basal LH release and LH cell content in vitro were drastically reduced in GnRH agonist-suppressed cells (P<0·001). However, basal FSH release and FSH cell content were approximately twofold higher than in control cells (P<0·001). Irrespective of whether the cells had been desensitized to GnRH, inhibin and oestradiol were both found to suppress basal FSH release and FSH cell content in a dose-dependent fashion (P<0·001). Although inhibin had no effect on basal release of LH from control cells, it markedly enhanced GnRH-induced release (P<0·001). In contrast, inhibin increased (P<0·001) basal LH release from GnRH agonist-suppressed cells (which were unresponsive to the GnRH challenge). Inhibin had no overall effect on total LH content/well for either control or GnRH agonist-suppressed cells. Treatment with oestradiol, on the other hand, reduced total LH content/well, an effect which was more pronounced with GnRH agonist-suppressed cells (−44%; P<0·001) than with control cells (−14%, P<0·01). Whereas in control cells activin had no significant effect on any aspect of FSH production examined, in GnRH agonist-treated cells activin enhanced basal FSH release, residual cell content and total FSH content/well (P<0·001). Altering GnRH receptor status also modified the LH response to activin. With control cells activin increased basal release (P<0·001), decreased GnRH-induced release (P<0·001) and increased total LH content/well (P<0·001). With GnRH agonist-treated cells, however, activin had a uniform inhibitory effect on each aspect of LH production examined (P<0·001 in each case). It was concluded that desensitization of ovine gonadotrophs to GnRH by chronic agonist treatment results in a paradoxical enhancement of FSH output in vitro but has little effect on the responsiveness of the cells (in terms of gonadotrophin release and content) to either inhibin or oestradiol. In contrast, GnRH agonist treatment leads to qualitative changes in cellular reponsiveness to activin. Journal of Endocrinology (1994) 140, 483–493

Circulating gonadotrophin surge-attenuating factor from superovulated women suppresses in vitro gonadotrophin-releasing hormone self-priming

1994 ◽  
Vol 143 (1) ◽  
pp. 45-54 ◽  
Author(s):  
P A Fowler ◽  
P Cunningham ◽  
M Fraser ◽  
F MacGregor ◽  
B Byrne ◽  
...  
Keyword(s):  
Follicular Fluid ◽  
Peripheral Circulation ◽  
Basal Secretion ◽  
Releasing Hormone ◽  
Significant Difference ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Marked Suppression ◽  
Stimulation Of

Abstract A penfusion system based on ovine pituitary tissue explants was used to investigate the effects of follicular fluid (hFF) and serum from superovulated women on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH). The specific aims of the study were to determine both if gonadotrophin surge-attenuating factor (GnSAF) bioactivity is present in the peripheral circulation as well as in the follicles of superovulated women and if GnSAF suppresses GnRH self-priming in vitro. Two pulses of GnRH, 1 h apart, produced marked peaks in LH secreted from control chambers, with GnRH self-priming evident in the significant difference between the first (134·4±1·7–232·1±24·0% of basal secretion) and second (183·9±15·8–313·9±14·0% of basal secretion) LH peaks. Both follicular fluid and serum pooled from two different groups of women produced marked suppression of the first (unprimed) and second (primed) LH peaks. The hFF reduced the first LH peak to 69·6±7·8 and 60·2±9·7% and the second LH peak to 57·4±6·7 and 42·6±6·5% of control LH secretion. Overall, the serum reduced the first and second LH peaks to 76·8±4·2 and 62·9±3·6% of control respectively. These results demonstrated that GnSAF bioactivity suppresses GnRH self-priming, and is present in both the peripheral circulation and hFF. The same material administered to dispersed ovine pituitary monolayers produced similar marked suppression of GnRH-induced LH secretion, with approximately 50-fold less GnSAF bioactivity in serum compared with hFF. Combined doses of oestradiol and progesterone, or hFF from large follicles containing little GnSAF, produced stimulation of GnRH-induced LH secretion and GnRH self-priming (second peaks 78·1±38·9 and 27·4±15·7% respectively higher than first peaks). Thus, in conclusion, GnSAF in hFF and serum markedly attenuated both unprimed and primed pituitary response to GnRH, virtually abolishing the GnRH self-priming effect. Journal of Endocrinology (1994) 143, 45–54

Sign in / Sign up

Export Citation Format

Share Document