Fertility control in female eastern grey kangaroos using the GnRH agonist deslorelin. 2. Effects on behaviour

2006 ◽  
Vol 33 (1) ◽  
pp. 47 ◽  
Author(s):  
R. Woodward ◽  
M. E. Herberstein ◽  
C. A. Herbert
Keyword(s):  
Gnrh Agonist ◽  
Slow Release ◽  
Fertility Control ◽  
Management Option ◽  
Control Techniques ◽  
Acceptable Alternative ◽  
Behavioural Effects ◽  
Effective Inhibition ◽  
Immunological Approach ◽  
Gonadotrophin Releasing Hormone

In recent years fertility control has been proposed as an ethically acceptable alternative to lethal control techniques when managing overabundant kangaroo populations. A promising non-steroidal, non-immunological approach to contraception in female kangaroos involves the use of slow-release implants containing the gonadotrophin-releasing hormone (GnRH) agonist deslorelin. The practicality of using deslorelin implants as a management option is dependant on its effective inhibition of reproduction without negative physical or behavioural side-effects. This study investigated the behavioural effects of deslorelin implants in female eastern grey kangaroos. Treatment had no detectable effects on crepuscular activity. Alterations in the frequency of sexual interactions were observed in deslorelin-treated females, with a behavioural oestrus induced ~3 days after combined removal of pouch young and deslorelin administration. Copulation was observed during this early oestrous period, but conception was not achieved and pouch young were not observed in any treated females. Control females gave birth within 69.6 ± 10.4 days (mean ± s.e.m., n = 9) of placebo implant administration. The first births observed in treated animals were on Days 510, 637 and 643 after treatment. The remaining seven treated animals had not bred by the end of the study, a period of 647 days.

Fertility control in female eastern grey kangaroos using the GnRH agonist deslorelin. 1. Effects on reproduction

2006 ◽  
Vol 33 (1) ◽  
pp. 41 ◽  
Author(s):  
C. A. Herbert ◽  
T. E. Trigg ◽  
D. W. Cooper
Keyword(s):  
Urban Areas ◽  
East Coast ◽  
Slow Release ◽  
Fertility Control ◽  
Minimum Duration ◽  
Reproductive Management ◽  
Adult Females ◽  
Gonadotrophin Releasing Hormone ◽  
Negative Side Effects ◽  
Control Technologies

Eastern grey kangaroos are widespread on the east coast of Australia and frequently reach high densities in reserves and parkland near urban areas. Management of these populations is highly contentious and non-lethal fertility-control technologies are sought as an alternative option to manage population size. This study evaluated the potential of slow-release gonadotrophin-releasing hormone agonist (deslorelin) implants to inhibit reproduction in female kangaroos. Deslorelin treatment effectively inhibited reproduction in adult females for periods of 559 ± 111 days (n = 6) and 651 ± 21 days (n = 5) after administration of one or two 10-mg implants respectively. Animals treated with the lower dosage tended to resume breeding earlier than those that received a total of 20 mg of deslorelin (minimum duration of 18 months). Deslorelin treatment had no effect on blastocyst reactivation in a single treated female and repeat treatment had no negative side-effects. This study has demonstrated that slow-release deslorelin implants can successfully inhibit reproduction for extended periods in the female eastern grey kangaroos. This approach may have potential application in reproductive management of problem kangaroo populations.

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

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

scholarly journals Evaluation of adenomyosis after gonadotrophin-releasing hormone agonist therapy using ultrasound post-processing imaging: a pilot study

2020 ◽  
Vol 48 (6) ◽  
pp. 030006052092005
Author(s):  
Szu-Yuan Chou ◽  
Cindy Chan ◽  
Yu-Chieh Lee ◽  
Tzu-Ning Yu ◽  
Chii-Ruey Tzeng ◽  
...  
Keyword(s):  
Image Analysis ◽  
Gnrh Agonist ◽  
Post Treatment ◽  
Ca 125 ◽  
Ultrasound Images ◽  
Analysis Software ◽  
Image Analysis Software ◽  
Computer Aided ◽  
Gonadotrophin Releasing Hormone ◽  
Pre Treatment

Objective We explored a method for the quantitative sonographic analysis of myometrial texture using computer-aided image analysis software to assess outcomes following treatment with gonadotrophin-releasing hormone (GnRH) agonist for adenomyosis in women with infertility. Method Data for patients with ultrasound images of the myometrium obtained at Taipei Medical University Hospital from 1 September 2018 to 5 April 5 2019 were analyzed. Only 10 patients with 20 ultrasound images matched the eligibility criteria. The images were divided into pre-treatment (n = 10) and post-treatment images (n = 10) and quantitative grayscale histograms were obtained from the ultrasound images using publicly available ImageJ computer-aided image analysis software. We analyzed the differences between the pre- and post-treatment images using the Mann–Whitney test and compared the results with outcomes assessed by serum CA-125 levels. Results Image analysis of the grayscale histograms revealed significant differences between before and after treatment. The classification of the myometrium pre-treatment and post-treatment was similar using CA-125 and histogram grayscale analysis. Conclusion Computer-aided image analysis of grayscale histograms of the myometrium obtained from ultrasound images is an alternative method for assessing myometrial conditions after GnRH agonist treatment in patients with adenomyosis.

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

Effects of pituitary-gonadal suppression with a gonadotrophin-releasing hormone agonist on fetal gonadotrophin secretion, fetal gonadal development and maternal steroid secretion in the sheep

1994 ◽  
Vol 141 (2) ◽  
pp. 317-324 ◽  
Author(s):  
G B Thomas ◽  
A S McNeilly ◽  
F Gibson ◽  
A N Brooks
Keyword(s):  
Gnrh Agonist ◽  
Fetal Development ◽  
Plasma Concentrations ◽  
Gonadal Development ◽  
Maternal Circulation ◽  
Biodegradable Implant ◽  
Steroid Secretion ◽  
Releasing Hormone ◽  
Pituitary Glands ◽  
Gonadotrophin Releasing Hormone

Abstract In order to investigate the regulation of the hypothalamo-pituitary-gonadal axis during fetal development, sheep fetuses at day 70 of gestation were implanted subcutaneously with a biodegradable implant containing the longacting gonadotrophin-releasing hormone (GnRH) agonist, buserelin. The treatment of fetuses with a GnRH agonist throughout the last half of gestation (term=145 days) abolished the increase in plasma LH concentrations that was seen in 2-day-old control lambs in response to an injection of GnRH. This attenuated response was associated with corresponding reductions in the pituitary content of LH and FSH. Immunolocalization studies revealed that pituitary glands from newborn lambs implanted with a GnRH agonist during fetal development were devoid of immunopositive LH- and FSH-containing cells. At birth the testicular weights of GnRH agonist-treated ram lambs were significantly decreased by 40% when compared with controls. This was associated with a 45% reduction in the total number of Sertoli cells per testis. In newborn ewe lambs GnRH agonist treatment had no effect on ovarian weight or on the morphological appearance of the ovaries. GnRH agonist treatment had no effect on the plasma concentrations of progesterone and oestrone in the maternal circulation or on the length of gestation. These results show (1) that GnRH positively regulates the synthesis and secretion of gonadotrophins in the fetus, (2) that reduced fetal gonadotrophic support during the last half of gestation results in a reduction in testicular growth, and (3) that fetal gonadotrophins do not affect maternal steroid secretion. Journal of Endocrinology (1994) 141, 317–324

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