EFFECT OF 20α-HYDROXYY-4-PREGNEN-3-ONE ON LUTEINIZING HORMONE SECRETION IN THE FEMALE RABBIT

1977 ◽  
Vol 84 (1) ◽  
pp. 45-50 ◽  
Author(s):  
E. V. YoungLai

ABSTRACT Experiments were performed in the rabbit to determine whether 20α-hydroxy-4-pregnen-3-one (20-OHP) can maintain luteinizing hormone (LH) secretion after injections of LH-releasing hormone (LH-RH). Female rabbits were castrated at least 2 weeks prior to investigation. On the day before LH-RH injection they were cannulated and a dose of oestradiol benzoate (OeB), 100 μg/kg, given intramuscularly. LH-RH, 500 ng/kg, was injected as a bolus via the cannula and 20-OHP, 100 μg/kg and 2.5 mg/kg, injected intramuscularly immediately after. Blood was withdrawn at intervals for up to 5½ h after LH-RH injection. LH secretion dropped to pre-stimulation levels within 3 h after LH-RH alone or in combination with 20-OHP. Administration of LH-RH to oestrogen primed intact females also gave a peak of LH which returned to pre-stimulation levels within 3 h. However, mating seemed to maintain LH levels for a greater period of time.

2009 ◽  
Vol 54 (No. 3) ◽  
pp. 97-110 ◽  
Author(s):  
P. Podhorec ◽  
J. Kouril

Gonadotropin-releasing hormone in Cyprinidae as in other Vertebrates functions as a brain signal which stimulates the secretion of luteinizing hormone from the pituitary gland. Two forms of gonadotropin-releasing hormone have been identified in cyprinids, chicken gonadotropin-releasing hormone II and salmon gonadotropin-releasing hormone. Hypohysiotropic functions are fulfilled mainly by salmon gonadotropin-releasing hormone. The only known factor having an inhibitory effect on LH secretion in the family Cyprinidae is dopamine. Most cyprinids reared under controlled conditions exhibit signs of reproductive dysfunction, which is manifested in the failure to undergo final oocyte maturation and ovulation. In captivity a disruption of endogenous gonadotropin-releasing hormone stimulation occurs and sequentially that of luteinizing hormone, which is indispensible for the final phases of gametogenesis. In addition to methods based on the application of exogenous gonadotropins, the usage of a method functioning on the basis of hypothalamic control of final oocyte maturation and ovulation has become popular recently. The replacement of natural gonadotropin-releasing hormones with chemically synthesized gonadotropin-releasing hormone analogues characterized by amino acid substitutions at positions sensitive to enzymatic degradation has resulted in a centuple increase in the effectiveness of luteinizing hormone secretion induction. Combining gonadotropin-releasing hormone analogues with Dopamine inhibitory factors have made it possible to develop an extremely effective agent, which is necessary for the successful artificial reproduction of cyprinids.


1983 ◽  
Vol 99 (1) ◽  
pp. 1-8 ◽  
Author(s):  
T. R. Koiter ◽  
G. C. J. van der Schaaf-Verdonk ◽  
H. Kuiper ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling

The effects of steroid-free bovine follicular fluid (bFF) and sodium phenobarbitone on spontaneous LH releasing hormone (LHRH)-induced secretion of FSH and LH were studied in ovariectomized rats. Luteinizing hormone releasing hormone was administered by infusion to rats anaesthetized with phenobarbitone. Bovine follicular fluid reduced FSH release and synthesis. Luteinizing hormone release remained unaffected after bFF treatment. Phenobarbitone reduced both FSH and LH release. The observed suppressive effects of bFF and phenobarbitone on FSH secretion were additive, suggesting that the basal release of FSH has an LHRH-dependent and an LHRH-independent component. Furthermore, bFF did not affect pituitary responsiveness of LH secretion to LHRH and reduced the responsiveness of FSH secretion only when administered some time before the LHRH challenge. The present observations support the view that in the ovariectomized rat the pituitary gland is the only site of action of inhibin-like activity as present in bFF.


1988 ◽  
Vol 66 (1) ◽  
pp. 38-42 ◽  
Author(s):  
E. V. YoungLai ◽  
M. Wilkinson ◽  
N. Thompson ◽  
A. Byrne

To examine the role of opioid neurons on luteinizing hormone (LH) secretion in the female rabbit, we determined LH release at timed intervals after naloxone administration to rabbits aged 25–150 days. The LH response to naloxone (10 mg/kg) was not significantly elevated until day 43 when LH rose 76–113% above basal levels at 40–80 min. In 56-day-old females the corresponding increase was 160% at 15 min and in 65- to 67-day-olds it was 154%. From 70 to 80 days of age the LH response was blunted and no significant elevations could be elicited. By contrast, naloxone-induced LH increases were again evident when rabbits were older than 100 days. At all ages no significant change in FSH concentrations was observed. In the adult females, naloxone at 2.5, 5, and 10 mg/kg caused increases in LH secretion which occasionally were high enough to induce ovulation as exemplified by elevated serum progesterone 4 days later. These data suggest that opioid peptides may be involved in the prepubertal rise in LH and in the normal inhibition of adult secretion in the female rabbit.


1977 ◽  
Vol 72 (2) ◽  
pp. 121-126 ◽  
Author(s):  
G. A. SCHUILING ◽  
H. P. GNODDE

SUMMARY Oestrogen-induced changes in luteinizing hormone secretion, caused by continuous infusions of luteinizing hormone releasing hormone (LH-RH), appear to depend on the duration of exposure of the pituitary gland to the releasing hormone. The initial oestrogen-induced depression of the potential response of the pituitary gland to LH-RH, which always seems to occur, does not necessarily turn into an enhancement of this potential response. It is suggested that this may be due to the fact that the response of the pituitary gland to LH-RH infusions is a continuously changing parameter influenced by oestrogen.


1983 ◽  
Vol 99 (2) ◽  
pp. 301-310 ◽  
Author(s):  
S. C. Wilson ◽  
P. G. Knight ◽  
F. J. Cunningham

Treatment of intact cockerels with the synthetic antioestrogen tamoxifen caused a significant increase in the plasma concentration of LH. In contrast, passive immunization with an antiserum raised against oestradiol-17β did not lead to an increase in plasma LH. A pronounced depressive effect of injections of 0·1 mg testosterone propionate (TP) or 0·1 mg oestradiol benzoate (OB) on plasma concentrations of LH was prevented by tamoxifen. Furthermore, a pronounced rise in the concentration of LH releasing hormone in the posterior hypothalamus after the injection of cockerels with OB was completely inhibited by tamoxifen. Neither 0·1 nor 0·5 mg androstenedione modified the concentration of LH in plasma. A dose of 0·05 mg TP, which failed to depress the concentration of LH in plasma of intact cockerels, caused a marked fall in plasma LH in castrated cockerels. Tamoxifen itself exhibited weak oestrogen agonist activity in castrated cockerels by causing a reduction in the concentration of LH in plasma. However, tamoxifen prevented any further depressive effect on LH resulting from the injection of TP. These findings suggest that testosterone exerts an inhibitory influence on LH secretion at the central neural level, partially at least, by means of the product of its aromatization, oestradiol-17β.


1982 ◽  
Vol 92 (3) ◽  
pp. 389-395 ◽  
Author(s):  
TAKASHI HIGUCHI ◽  
MASAZUMI KAWAKAMI

Ovariectomized rats with neural deafferentation at the level of the posterior border of the anterior hypothalamic area (AC rats) were used to re-evaluate the direct feedback effect of oestrogen on the regulation of LH secretion by the pituitary gland. Synthetic LH releasing hormone (LH-RH; 300 ng/kg), injected at 30-min intervals into AC rats with undetectable basal LH, induced pulsatile increase of serum LH concentrations. Oestradiol-17β (5 μg), administered i.v. just before the first LH-RH injection, significantly decreased the LH response to a second injection of LH-RH given 30 min later and to subsequent injections. Maximal inhibition was 58%. Oestradiol-17β (5 μg) given i.v. to control ovariectomized rats decreased serum LH concentrations 40 min after administration; the maximum reduction being 52%. An s.c. injection of oestradiol benzoate (5 μg) increased pituitary responsiveness to LH-RH by the next day in AC rats but decreased serum LH levels in control ovariectomized rats. These results indicate that acute inhibitory and chronic facilitatory effects of oestrogen on LH secretion are exerted at the pituitary gland, without a change in LH-RH secretion. The prolonged inhibitory effect of oestrogen is at the level of the hypothalamus and causes a reduction in LH-RH secretion.


1983 ◽  
Vol 102 (4) ◽  
pp. 499-504 ◽  
Author(s):  
M. J. D'Occhio ◽  
B. D. Schanbacher ◽  
J. E. Kinder

Abstract. The acute castrate ram (wether) was used as an experimental model to investigate the site(s) of feedback on luteinizing hormone (LH) by testosterone, dihydrotestosterone and oestradiol. At the time of castration, wethers were implanted subdermally with Silastic capsules containing either crystalline testosterone (three 30 cm capsules), dihydrotestosterone (five 30 cm capsules) or oestradiol (one 6.5 cm capsule). Blood samples were taken at 10 min intervals for 6 h 2 weeks after implantation to determine serum steroid concentrations and to characterize the patterns of LH secretion. Pituitary LH response to exogenous LRH (5 ng/kg body weight) were also determined at the same time. The steroid implants produced serum concentrations of the respective hormones which were either one-third (testosterone) or two-to-four times (dihydrotestosterone, oestradiol) the levels measured in rams at the time of castration. Non-implanted wethers showed rhythmic pulses of LH (pulse interval 40–60 min) and had elevated LH levels (16.1 ± 1.6 ng/ml; mean ± se) 2 weeks after castration. All three steroids suppressed pulsatile LH release and reduced mean LH levels (to below 3 ng/ml) and pituitary LH responses to LRH. Inhibition of pulsatile LH secretion by all three steroids indicated that testosterone as well as its androgenic and oestrogenic metabolites can inhibit the LRH pulse generator in the hypothalamus. Additional feedback on the pituitary was indicated by the dampened LH responses to exogenous LRH.


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