Effect of decapitation and chronic in-vivo treatment with a gonadotrophin-releasing hormone agonist on testicular steroidogenesis in the rat fetus

1992 ◽  
Vol 133 (2) ◽  
pp. 245-251 ◽  
Author(s):  
R. Habert
Keyword(s):  
Gnrh Agonist ◽  
Leydig Cells ◽  
Maternal Plasma ◽  
Plasma Testosterone ◽  
Fetal Life ◽  
Rat Fetus ◽  
Control Female ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone

ABSTRACT To study the effect of in-vivo gonadotrophin-releasing hormone (GnRH) treatment on testicular testosterone production during late fetal life in the rat, 18·5-, or 20·5-day-old fetuses were decapitated and injected with either long-acting microcapsules containing the GnRH agonist d-Trp-6-GnRH or vehicle only. Two days later, fetal and maternal plasma was collected and fetal testes were removed and incubated for 6 h in medium with either 100 ng LH/ml or without LH. The GnRH agonist concentrations in the plasma of GnRH-treated decapitated male fetuses were comparable in the two age-related groups (5 nmol/l). After treatment of the fetus with d-Trp-6-GnRH, the agonist was recovered in maternal plasma, showing that this peptide can cross the fetal–maternal barrier. In 22·5-day-old decapitated vehicle-treated male fetuses, the plasma testosterone level dropped to that observed in control female fetuses, and treatment of decapitated male fetuses with the GnRH agonist did not further reduce it. At both days 20·5 and 22·5, basal in-vitro testosterone secretion by testes from decapitated vehicle-treated fetuses was lower than secretion by testes from intact control fetuses from the same litter, but LH-stimulated secretion was similar in both groups. Both basal and LH-stimulated secretion by testes from GnRH-treated decapitated fetuses was lower than secretion by testes from vehicle-treated decapitated fetuses and larger reductions were measured on day 22·5 than on day 20·5 (−48 vs −18% for basal secretion, and −76 vs −40% for LH-stimulated secretion). These results suggest that, in contrast to immature Leydig cells, fetal Leydig cells are not desensitized to gonadotrophic stimulation after hypophysial deprivation, and that, in the rat, a negative testicular response to a putative intratesticular GnRH or to some other factor using the same intracellular pathway is established during late fetal life. Journal of Endocrinology (1992) 133, 245–251

In vivo acute testicular testosterone response to injection of luteinizing hormone in the rat fetus

1993 ◽  
Vol 128 (3) ◽  
pp. 268-273 ◽  
Author(s):  
René Habert
Keyword(s):  
Plasma Concentration ◽  
Luteinizing Hormone ◽  
Leydig Cells ◽  
Time Dependent ◽  
Fetal Life ◽  
Dependent Manner ◽  
Adult Rats ◽  
Rat Fetus ◽  
Age Related

The acute in vivo testosterone response to LH stimulation and its change during late fetal life were determined in the rat. In 18.5-day-old fetuses, testicular testosterone content was increased in a dose-and time-dependent manner after fetal subcutaneous LH injection. The maximum response was small: the testicular content and plasma concentration were increased by 200% and 2 50% over basal values respectively, while they were increased 1100% and 1200% in adult rats. Similarly, comparable low responses were obtained after subcutaneously injecting the fetuses with human chorionic gonadotropin (hCG) and after injecting LH into the vitelline vein. Between days 18.5 and 21.5 of fetal life, the testosterone levels in the testis and plasma of uninjected or PBS-injected fetuses decreased and were comparable in both groups. In maximally LH-stimulated fetuses, the testicular content did not change with age, and plasma concentration was lower on day 21.5 than on day 18.5. Since the number of Leydig cells increases 1.5 to 2-fold between days 18.5 and 21.5, these results show an age-related decrease in basal and maximally LH-stimulated in vivo testosterone secretions per Leydig cell during late fetal life.

Effect of long-term inhibition of gonadotrophin secretion by the gonadotrophin-releasing hormone agonist, buserelin, on sex steroid secretion and ovarian morphology in polycystic ovary syndrome

1990 ◽  
Vol 125 (2) ◽  
pp. 317-325 ◽  
Author(s):  
A. F. Macleod ◽  
M. J. Wheeler ◽  
P. Gordon ◽  
C. Lowy ◽  
P. H. Sönksen ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Gnrh Agonist ◽  
Polycystic Ovary ◽  
Normal Subjects ◽  
Sex Hormone Binding Globulin ◽  
Plasma Testosterone ◽  
Ovary Syndrome ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone

ABSTRACT In order to investigate the effect of long-term suppression of the gonadotrophin axis in polycystic ovary syndrome, eight affected subjects were given s.c. infusions of gonadotrophin-releasing hormone (GnRH) agonist buserelin for 12 weeks. Hormone measurement and ultrasound studies were carried out weekly, from 6 weeks before to 12 weeks after administration of buserelin. An overnight dexamethasone-suppression test was carried out before and after treatment. Maximal suppression of LH to below the lower limit of that in normal subjects occurred after 6 weeks of treatment with buserelin. Plasma testosterone and androstenedione fell to normal levels during the infusion but reached pretreatment levels during the follow-up period. There was no effect of buserelin on plasma dehydroepiandrosterone sulphate or sex hormone-binding globulin. Ovarian size decreased significantly during the infusion with the disappearance of cysts in six subjects. After cessation of buserelin therapy, there was rapid and spontaneous ovulation which occurred within 3 weeks in all subjects. The results suggest that treatment with this GnRH agonist facilitates ovulation in this condition. Journal of Endocrinology (1990) 125, 317–325

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

Relationships between plasma progesterone levels and testicular testosterone production in the rat fetus: effects of maternal ovariectomy

1986 ◽  
Vol 108 (3) ◽  
pp. 361-367 ◽  
Author(s):  
R. Habert ◽  
R. Picon
Keyword(s):  
Plasma Concentrations ◽  
Maternal Plasma ◽  
Plasma Testosterone ◽  
Rat Fetus ◽  
Plasma Progesterone ◽  
Fetal Plasma ◽  
Testosterone Production ◽  
Fetal Rat

ABSTRACT The present study was performed to examine whether circulating progesterone regulates testicular testosterone production in the fetal rat. Progesterone levels in fetal plasma were found to increase from day 14·5 to day 16·5; thereafter they reached a plateau between days 16·5 and 18·5 (80 nmol/l) and decreased threefold between days 18·5 and 21·5. The addition of progesterone, within the range of normal plasma concentrations, induced a dose-dependent increase in testosterone produced in vitro by the testes on days 16·5 and 18·5 but not on day 20·5. However, in 18·5-day-old fetuses, individual plasma progesterone levels were not correlated with testicular testosterone production in vivo and in vitro. Furthermore, maternal bilateral ovariectomy induced a significant fall in plasma progesterone in 18·5-day-old fetuses; this was not associated with a reduction in plasma testosterone nor in testicular testosterone content, although the amount of testosterone secreted by the testis incubated in vitro was slightly but significantly reduced. It is concluded that circulating progesterone does not regulate testicular testosterone production in vivo although the testis may use plasma progesterone as a substrate. On day 18·5 after maternal ovariectomy, the decrease in plasma progesterone levels was similar in fetuses and mothers, suggesting that most fetal progesterone originates from maternal plasma. J. Endocr. (1986) 108, 361–367

THE EFFECT OF GONADOTROPHIN RELEASING HORMONE ON PITUITARY-GONADAL FUNCTION IN KLINEFELTER'S SYNDROME

1976 ◽  
Vol 83 (4) ◽  
pp. 829-838 ◽  
Author(s):  
A. G. H. Smals ◽  
P. W. C. Kloppenborg ◽  
R. M. Lequin ◽  
Th. J. Benraad
Keyword(s):  
Leydig Cells ◽  
Bolus Injection ◽  
Plasma Testosterone ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Releasing Hormone ◽  
Basal Plasma ◽  
Gonadotrophin Releasing Hormone ◽  
The Mean ◽  
Lh Rh

ABSTRACT The mean basal plasma LH and FSH levels in 8 patients with Klinefelter's syndrome were respectively 5 and 15-fold higher than in 8 eugonadal males, whereas plasma testosterone concentration were half the normal value After an intravenous bolus injection of gonadotrophin releasing hormone (100 μg of LH-RH) the gonadotrophin increase in the Klinefelter patients was more marked than in the control subjects, but in both groups the plasma testosterone levels remained essentially unchanged. In contrast to the bolus injection, an 8 h infusion of LH-RH after the bolus elicited a significant plasma testosterone increase in both the eugonadal males (59%) and the Klinefelter patients (51%). These findings indicate that despite an impressive endogenous hypergonadotrophism, Leydig cells in Klinefelter's syndrome can still respond to a sustained further increase of these endogenous gonadotrophins and thus still have functional reserve.

Suppression of pituitary-testis function in rats treated neonatally with a gonadotrophin-releasing hormone agonist and antagonist: acute and long-term effects

1989 ◽  
Vol 123 (1) ◽  
pp. 83-91 ◽  
Author(s):  
K.-L. Kolho ◽  
I. Huhtaniemi
Keyword(s):  
Body Weight ◽  
Gnrh Agonist ◽  
Gnrh Antagonist ◽  
Long Term Effects ◽  
Adult Rats ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Accessory Sex Organs ◽  
Gonadotrophin Releasing Hormone

ABSTRACT The acute and long-term effects of pituitary-testis suppression with a gonadotrophin-releasing hormone (GnRH) agonist, d-Ser(But)6des-Gly10-GnRH N-ethylamide (buserelin; 0·02, 0·1, 1·0 or 10 mg/kg body weight per day s.c.) or antagonist, N-Ac-d-Nal(2)1,d-p-Cl-Phe2,d-Trp3,d-hArg(Et2)6,d-Ala10-GnRH (RS 68439; 2 mg/kg body weight per day s.c.) were studied in male rats treated on days 1–15 of life. The animals were killed on day 16 (acute effects) or as adults (130–160 days; long-term effects). Acutely, the lowest dose of the agonist decreased pituitary FSH content and testicular LH receptors, but with increasing doses pituitary and serum LH concentrations, intratesticular testosterone content and weights of testes were also suppressed (P< 0·05–0·01). No decrease was found in serum FSH or in weights of accessory sex organs even with the highest dose of the agonist, the latter finding indicating continuing secretion of androgens. The GnRH antagonist treatment suppressed pituitary LH and FSH contents and serum LH (P< 0·05–0·01) but, as with the agonist, serum FSH remained unaltered. Testicular testosterone and testis weights were decreased (P <0·01) but testicular LH receptors remained unchanged. Moreover, the seminal vesicle and ventral prostate weights were reduced, in contrast to the effects of the agonists. Pituitary LH and FSH contents had recovered in all adult rats treated neonatally with agonist and there was no effect on serum LH and testosterone concentrations or on fertility. In contrast, in adult rats treated neonatally with antagonist, weights of testis and accessory sex organs remained decreased (P <0·01–0·05) but hormone secretion from the pituitary and testis had returned to normal except that serum FSH was increased by 80% (P <0·01). Interestingly, 90% of the antagonist-treated animals were infertile. It is concluded that treatment with a GnRH agonist during the neonatal period does not have a chronic effect on pituitary-gonadal function. In contrast, GnRH antagonist treatment neonatally permanently inhibits the development of the testis and accessory sex organs and results in infertility. Interestingly, despite the decline of pituitary FSH neonatally, neither of the GnRH analogues was able to suppress serum FSH values and this differs from the concomitant changes in LH and from the effects of similar treatments in adult rats. Journal of Endocrinology (1989) 123, 83–91

THE EFFECT OF CYPROTERONE ACETATE ON THE PLASMA GONADOTROPHIN RESPONSE TO GONADOTROPHIN RELEASING HORMONE

1976 ◽  
Vol 81 (3) ◽  
pp. 680-684 ◽  
Author(s):  
Richard A. Donald ◽  
Eric A. Espiner ◽  
R. John Cowles ◽  
Joy E. Fazackerley
Keyword(s):  
Testosterone Level ◽  
Cyproterone Acetate ◽  
Luteinising Hormone ◽  
Follicle Stimulating Hormone ◽  
Plasma Testosterone ◽  
Plasma Testosterone Level ◽  
Releasing Hormone ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Male Patients

ABSTRACT Cyproterone acetate (100–150 mg daily) was administered to 8 male patients with excessive libido. Within 3 months a significant fall (P < 0.02) in plasma testosterone was demonstrated. The plasma luteinising hormone (LH) and follicle stimulating hormone (FSH) responses to gonadotrophin releasing hormone (LH/FSH-RH) were also significantly impaired (P < 0.05). A direct correlation between the resting plasma testosterone level and the LH response to LH/FSH-RH was demonstrated (r = 0.743). It is concluded that the fall in plasma testosterone levels in patients receiving cyproterone acetate may be attributed to suppression of LH release, rather than an antiandrogen effect on the testis or hypothalamus.

Immunisation of male mice with a plasmid DNA vaccine encoding gonadotrophin releasing hormone (GnRH-I) and T-helper epitopes suppresses fertility in vivo

Vaccine ◽  
2007 ◽  
Vol 25 (18) ◽  
pp. 3544-3553 ◽  
Author(s):  
Mohammad A.H. Khan ◽  
Valerie A. Ferro ◽  
Shinsuke Koyama ◽  
Yukiko Kinugasa ◽  
Mihyon Song ◽  
...  
Keyword(s):  
Dna Vaccine ◽  
Plasmid Dna ◽  
Male Mice ◽  
T Helper ◽  
Releasing Hormone ◽  
Plasmid Dna Vaccine ◽  
Gonadotrophin Releasing Hormone
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