Retardation of preovulatory desensitization to negative oestrogen feedback: mechanism of the effect of progesterone in 5-day cyclic rats

1987 ◽  
Vol 114 (3) ◽  
pp. 409-414 ◽  
Author(s):  
F. Döcke ◽  
W. Rohde ◽  
R. Chaoui ◽  
J. Stürzebecher ◽  
G. Dörner
Keyword(s):  
Preoptic Area ◽  
Feedback Mechanism ◽  
Ovarian Cycle ◽  
Female Rats ◽  
Mediobasal Hypothalamus ◽  
Inhibiting Effect ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Lh Secretion ◽  
Follicle Maturation

ABSTRACT Recent studies have shown that oestrogen can induce desensitization to its own gonadotrophin-inhibiting effect in female rats by an action on the medial preoptic area (MPOA). Probably as a consequence of this action, sensitivity to the negative oestrogen feedback declines markedly between metoestrus and dioestrus of the 4-day ovarian cycle. To study this desensitization process in 5-day cyclic rats, females exhibiting regular 5-day vaginal cyclicity were ovariectomized on consecutive days of the cycle, injected with oestradiol benzoate (OB) or oil on the day of ovariectomy and autopsied 24 h after the injection. Estimation of the serum concentration of LH revealed that desensitization to negative oestrogen feedback occurred only between day 2 of dioestrus and pro-oestrus, i.e. 2 days later than in females with a 4-day cycle. In the latter animals, an injection of progesterone in metoestrus or early dioestrus, which induced lengthening of the ovarian cycle for 1 day, delayed the onset of desensitization to a degree similar to that found in spontaneously 5-day cyclic rats. In acutely ovariectomized females, progesterone implants placed in the MPOA, but not those located in the mediobasal hypothalamus, increased the LH-inhibiting effect of low doses of OB. The results suggest that the prolonged secretion of progesterone recorded in 5-day cyclic rats retards follicle maturation and delays the forthcoming ovulation by acting, at least partly, on the MPOA and antagonizing the desensitizing effect of oestrogen. In this way, inhibition of gonadotrophin secretion by oestrogen is enhanced and the increase in tonic LH secretion necessary for the completion of follicle maturation is retarded. J. Endocr. (1987) 114, 409–414

Varying sensitivity to the negative oestrogen feedback during the ovarian cycle of female rats: evidence for the involvement of oestrogen and the medial preoptic area

1984 ◽  
Vol 102 (3) ◽  
pp. 287-294 ◽  
Author(s):  
F. Döcke ◽  
W. Rohde ◽  
P. Gerber ◽  
R. Chaoui ◽  
G. Dörner
Keyword(s):  
Preoptic Area ◽  
Medial Preoptic Area ◽  
Ovarian Cycle ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Adult Rats ◽  
Gonadotrophin Secretion ◽  
Arcuate Region ◽  
Lh Secretion ◽  
Follicle Maturation

ABSTRACT The gonadotrophic response to a single injection of oestradiol benzoate (OB) was studied in acutely ovariectomized adult rats during the different stages of a 4-day ovarian cycle. The results showed a sudden decline of the sensitivity to the gonadotrophin-inhibiting effect of OB between metoestrus and dioestrus. This desensitization to the negative oestrogen feedback was probably caused by an oestrogen action on the medial preoptic area (MPOA). In rats ovariectomized and implanted with OB in the MPOA in metoestrus, an s.c. injection of OB on the presumptive day of pro-oestrus did not lower the circulating LH and FSH levels, whereas a clear suppression of gonadotrophin secretion was seen in females implanted with cholesterol in the MPOA or implanted with OB in the hypothalamic ventromedial–arcuate region. Similar findings were obtained in rats which had been ovariectomized 3–4 weeks before implantation. A final experiment demonstrated that bilateral lesioning of the MPOA also reduced the sensitivity to the negative feedback action of oestrogen in long-term ovariectomized rats. In all experiments performed, diminution of the oestrogen-induced inhibition of LH secretion was more marked than that of suppression of FSH secretion. It is proposed that desensitization to the negative oestrogen feedback, probably resulting from an inhibitory oestrogen action on medial preoptic neurones, is a prerequisite for adequate gonadotrophic support of preovulatory follicle maturation in the presence of a continuously rising oestrogen concentration in the blood. J. Endocr. (1984) 102, 287–294

The inhibitory effect of opiates on gonadotrophin secretion is dependent upon gonadal steroids

1984 ◽  
Vol 102 (2) ◽  
pp. 133-141 ◽  
Author(s):  
R. Bhanot ◽  
M. Wilkinson
Keyword(s):  
Negative Feedback ◽  
Prolactin Secretion ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Inhibitory Effects ◽  
Endogenous Opiates ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Lh Secretion

ABSTRACT We have attempted to clarify the physiological involvement of endogenous opiates in the steroid-mediated control of gonadotrophin release. Our studies showed that there was an acute reduction in the inhibitory effects of endogenous opiates on LH and FSH release following gonadectomy in the rat. This was indicated by a significant reduction in the ability of naloxone to stimulate serum LH/FSH levels (sampled at 15 min) in 26-day-old female rats 48 h after ovariectomy. Luteinizing hormone was highly sensitive to the inhibitory effects of the synthetic met-enkephalin analogue, FK 33-824, at this time (sampled at 90 min). An unexpected observation was that long-term absence of gonadal steroids also disrupted the ability of exogenous opiates, FK 33-824 and morphine, to influence LH release. This was seen as an inability of FK 33-824 (1·0 or 3·0 mg/kg) to inhibit LH secretion. The effects of gonadectomy on opiate control of LH occurred at all developmental stages and were not due to a disruption of sexual maturation. Opiate involvement in prolactin secretion did not appear to be adversely affected by an absence of gonadal steroids. Another novel aspect of this work was that the opiatergic component in the control of gonadotrophin secretion could be reinstated in long-term gonadectomized rats by treatment with oestradiol benzoate or testosterone propionate. Similarly, priming with increasing dosages of oestradiol benzoate which resulted in progressively lower LH levels gave larger naloxone responses. This steroid–opiate interdependency suggests that the negative feedback influence of gonadal steroids on LH secretion is conveyed, in part, by hypothalamic opiate peptides. Our results therefore provide a neurochemical basis for gonadal steroid negative feedback. J. Endocr. (1984) 102, 133–141

THE MECHANISM OF THE INDUCTION OF OVULATION BY OESTROGENS

1965 ◽  
Vol 33 (3) ◽  
pp. 491-499 ◽  
Author(s):  
F. DÖCKE ◽  
G. DÖRNER
Keyword(s):  
Effective Dose ◽  
Corpus Luteum ◽  
Anterior Pituitary ◽  
Anterior Hypothalamus ◽  
Female Rats ◽  
Main Site ◽  
Induction Of Ovulation ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Electrolytic Lesions

SUMMARY To study the positive feed-back mechanism by which oestrogen induces corpus luteum formation, electrolytic lesions were placed in different parts of the anterior hypothalamus of prepubertal female rats which were then injected with oestradiol benzoate. Ovarian luteinization did not occur when the main parts of the suprachiasmatic nuclei or of the medial preoptic area had been destroyed. Oestradiol benzoate was implanted stereotaxically into the brain and the anterior pituitary of immature female rats. Whereas 1/25 of the subcutaneously effective dose had to be implanted into the anterior hypothalamus, 1/100 of the peripherally effective dose introduced into the adenohypophysis was sufficient to induce corpus luteum formation in most of the treated animals. The results suggest that, although the anterior hypothalamus is necessary for this positive feed-back mechanism, the anterior pituitary may be the main site of action of oestrogen. Oestrogen may increase the hypophysial sensitivity to the hypothalamic gonadotrophin-releasing factor. Thus an enhanced gonadotrophin secretion may result, sufficient for the induction of ovulation. The possibility is discussed that this positive feed-back mechanism is also essential for the induction of ovulation in women.

OESTROGEN AND THE CONTROL OF GONADOTROPHIN SECRETION IN THE IMMATURE RAT

1974 ◽  
Vol 63 (2) ◽  
pp. 285-298 ◽  
Author(s):  
F. DÖCKE ◽  
G. DÖRNER
Keyword(s):  
Wistar Rats ◽  
Short Term ◽  
Oestrogen Treatment ◽  
Immature Rat ◽  
Inhibiting Effect ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Female Wistar Rats ◽  
Implantation Method

SUMMARY Experiments were performed in female Wistar rats on the mode of action of oestrogen in affecting gonadotrophin secretion during infancy. Using an improved implantation method, former findings on a hypophysial site of oestrogen action in the Hohlweg effect were confirmed. The sensitivity to the ovulation-inducing effect of oestradiol benzoate (OB) increased as the rats approached the age of natural puberty. The first spontaneous ovulation could be suppressed by intrahypophysial, but not by intrahypothalamic, progesterone implants. A single s.c. injection or intracranial administration of OB at 25 or 26 days of age, although leading to premature vaginal opening (VO) and, in some of the animals, to one ovulation, did not induce true precocious puberty. To accelerate the onset of puberty, 0·05 μg OB/100 g body wt had to be injected daily from 5 days of age to VO, or from day 5 to day 10 and, additionally, from day 26 to VO. After long-term oestrogen treatment, the gonadotrophin-inhibiting effect of OB implanted into the middle hypothalamus from 26 to 34 days of age was significantly reduced in comparison with untreated control rats. A final experiment demonstrated that the first ovarian cycle was not prolonged after neonatal ovariectomy and implantation of ovaries at 24, 28 or 32 days of age. The results indicate that similar neurohormonal mechanisms are operational at the first pubertal and at later cyclic ovulations. They also indicate that the maturation of the gonadotrophin-controlling mechanisms continues during infancy in the absence of ovarian steroids. It can be accelerated in Wistar rats by long-term, but not by short-term prepubertal oestrogen treatment.

Dissociation between the ovarian factors controlling sexual receptivity and preovulatory secretion of LH in cyclic female rats

1987 ◽  
Vol 112 (1) ◽  
pp. 133-138 ◽  
Author(s):  
P. Södersten ◽  
P. Eneroth
Keyword(s):  
Sexual Behaviour ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Serum Progesterone ◽  
Lh Surge ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion ◽  
Intact Rats

ABSTRACT Ovariectomy and treatment with oestradiol benzoate (10 μg OB) on the day before behavioural oestrus eliminated the preovulatory surge of LH and reduced the level of sexual receptivity on the following day. Sexual behaviour, but not the LH surge, was restored by progesterone (0·5 mg) given 18 h later. Injection of OB on the day after behavioural oestrus induced a small release of LH and normal sexual behaviour on the following day. Ovariectomy on the day after behavioural oestrus reduced the stimulatory effect of OB on sexual behaviour and eliminated its weakly stimulatory effect on LH release. Sexual behaviour, but not the small LH surge, was restored in these animals by progesterone (0·5 mg) given 18 h later. Treatment of rats ovariectomized 2 days before the day of the LH surge with implants containing oestradiol or injections of oestradiol (1 μg) induced LH surges but the amplitudes of these LH surges were much smaller than those of the normal LH surge. Treatment of intact rats with OB increased serum progesterone levels 24 h later, an effect which was eliminated by ovariectomy. Injections of LH (20 μg) into intact rats on the day after behavioural oestrus also increased serum progesterone concentrations but failed to stimulate sexual behaviour. It is suggested that OB treatment of intact rats on the day after behavioural oestrus stimulates sexual behaviour by inducing a surge of LH secretion which activates ovarian secretion of progesterone. Thus, oestrogen and progesterone but not the LH surge are essential for sexual behaviour. Whereas oestradiol and progesterone restore normal sexual behaviour in ovariectomized rats, additional ovarian factors may be required for induction of normal LH surges. J. Endocr. (1987) 112, 133–138

The effects of steroidal and non-steroidal ovarian hormones on pituitary responsiveness to gonadotrophin surge-attenuating factor

1996 ◽  
Vol 150 (3) ◽  
pp. 413-422 ◽  
Author(s):  
B Byrne ◽  
P A Fowler ◽  
A Templeton
Keyword(s):  
Ovarian Hormones ◽  
Female Rats ◽  
High Dose ◽  
Additive Effects ◽  
Gonadotrophin Secretion ◽  
Sds Page ◽  
Wide Range ◽  
Lh Secretion ◽  
Late Follicular Phase

Abstract Primary pituitary cultures from adult female rats were used to investigate the effects of steroidal (oestradiol and progesterone) and non-steroidal (inhibin, follistatin) ovarian hormones on the suppressive actions of the ovarian factor gonadotrophin surge-attenuating factor (GnSAF) in the control of gonadotrophin secretion. The source of GnSAF was a chromatographic preparation from follicular fluid containing four distinct protein bands as resolved on SDS–PAGE. Oestradiol and progesterone added alone had no effect on gonadotrophin secretion but had a wide range of effects on the suppression of both LH and FSH secretion caused by the non-steroidal factors. Oestradiol, progesterone and oestradiol+progesterone enhanced the suppressive actions of GnSAF on GnRH-induced LH secretion (causing 19·3 ± 5·2% (P<0·05), 41·9 ± 3·4% (P<0·001) and 32·2 ± 5·3% (P<0·001) greater suppression than GnSAF alone). Progesterone and oestradiol+progesterone completely abolished the suppression of basal FSH secretion caused by inhibin (causing 157·1 ± 22·2%, P<0·001, and 160·9 ± 11·3%, P<0·001, stimulation compared with inhibin alone). Separately the steroids had no effect on the suppression of gonadotrophin secretion caused by follistatin. However, in combination, oestradiol+ progesterone potentiated the suppressive actions of follistatin on GnRH-induced LH secretion causing 29·9 ± 5·3% (P<0·05) greater suppression than follistatin alone. In combination, high-dose follistatin and GnSAF caused 31·1 ±6·5% (P<0·01) greater suppression than GnSAF alone. Thus in combination high-dose follistatin and GnSAF have additive effects on the suppression of GnRH-induced LH secretion. Recombinant human inhibin and GnSAF added in combination had little further effect compared with either alone suggesting that they may have a similar mechanism of action at the pituitary level. These results demonstrate that while FSH secretion in vitro is mainly controlled by inhibin and follistatin, LH secretion is affected by the presence of a whole range of factors. We have demonstrated that oestradiol and progesterone potentiate the suppressive actions of GnSAF in vitro. These data are compatible with the suggestion that in the late follicular phase it is falling levels of GnSAF that allow positive feedback of the steroids on the pituitary to elicit the LH surge, rather than increases in the stimulatory effects of the ovarian steroids overcoming GnSAF. The actions of GnSAF on the pituitary may be modulated by follistatin but it is unlikely that inhibin has any modulatory effects on the GnSAF-induced suppression of LH secretion. Journal of Endocrinology (1996) 150, 413–422

INHIBITION OF PROLACTIN SECRETION BY ERGOT ALKALOIDS

1975 ◽  
Vol 80 (3) ◽  
pp. 429-443 ◽  
Author(s):  
H. Nasr ◽  
O. H. Pearson
Keyword(s):  
Ergot Alkaloids ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Function Evaluation ◽  
Inhibiting Effect ◽  
Oestradiol Benzoate ◽  
Ovine Prolactin ◽  
Medical Therapeutics ◽  
Stimulation Of ◽  
Intact Rats

ABSTRACT The effect of various ergot alkaloids on prolactin (Pr) secretion in adult female rats was determined by radioimmunoassay. Ergocornine (ECO) and ergocristine (ECR) in doses of 0.25 to 1.0 mg lowered serum Pr markedly by 1 h with the effect persisting for 24 h at the larger doses. Several other ergots had similar effects while the dihydro derivatives had diverse responses. The pro-oestrous surge of Pr could be blocked by ECR or ECO without interfering with the oestrous cycle. ECO or ECR could suppress the rise in serum Pr induced by oestradiol benzoate (OeB) (5–50 μg) in oophorectomized rats. Perphenazine (PE) stimulation of Pr could be partially antagonized by ECO depending on dose and timing of injections. ECO 2 mg produced an abrupt cessation of lactation with concomitant fall in serum Pr, and ovine prolactin restored this function. Evaluation of pituitary Pr concentration in lactating and intact rats receiving ECO leads to the conclusion that release of Pr from the pituitary is affected. ECO 1 or 2 mg produced a regression of dimethylbenz(a)anthracene (DMBA) induced rat mammary tumours which could not be reversed by OeB 5 μg, with persisting low serum Pr. PE 1 mg was able to raise serum Pr and stimulated tumour growth. Several of the ergot alkaloids have a profound inhibiting effect on Pr secretion and may be used for studies on Pr action, as well as in medical therapeutics.

Influence of anti-oestrogens on gonadotrophin secretion in control and ACTH-infused immature rats

1984 ◽  
Vol 105 (3) ◽  
pp. 308-313 ◽  
Author(s):  
David R. Mann ◽  
Michael S. Blank ◽  
R. Sridaran ◽  
V. Daniel Castracane ◽  
Charles Eldridge ◽  
...  
Keyword(s):  
Serum Testosterone ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Constant Infusion ◽  
Simultaneous Treatment ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Immature Rats ◽  
Lh Secretion

Abstract. The objective of this study was to determine whether anti-oestrogens (nafoxidine, MER-25) would block the suppressive effects of ACTH on gonadotrophin secretion in immature rats. Female rats were castrated at 25–26 days of age, and an Alzet osmotic minipump containing ACTH (1–24) or saline was implanted in each animal. ACTH was administered at a rate of 1 IU/day by constant infusion. Beginning on the day of surgery, animals were injected daily for 5 days with 0.25, 5 or 25 μg/100 g body weight of nafoxidine or 5 mg MER-25 and sacrificed on the sixth day following castration. ACTH lowered serum LH concentrations and increased pituitary LH levels. Serum androstenedione concentrations were more than two times greater in ACTH-infused than in control rats, but serum oestrone levels were not affected. Serum testosterone and oestradiol concentrations in ACTH-infused rats remained below levels of detection. Administration of 0.25 μg of nafoxidine prevented the suppressive effects of ACTH on serum LH. Serum levels of LH in these animals were comparable to saline-treated controls (418 ± 94 vs 443 ± 73 ng/ml). The two higher doses of nafoxidine and MER-25 were ineffective in suppressing the actions of ACTH on serum LH. MER-25 reduced serum LH values in both controls and ACTH-infused rats. Serum FSH concentrations were not altered by ACTH or nafoxidine treatment. MER-25 elevated pituitary FSH concentrations in both control and ACTH-infused rats. These data suggest that the inhibitory effect of ACTH on LH secretion in immature rats is mediated by an oestrogenic steroid, since this action can be blocked by simultaneous treatment with a low dose of the anti-oestrogen, nafoxidine.

INFLUENCE OF AGE ON THE RELEASE OF LUTEINIZING HORMONE INDUCED BY OESTROGEN AND PROGESTERONE IN IMMATURE RATS

1972 ◽  
Vol 55 (1) ◽  
pp. 97-103 ◽  
Author(s):  
L. CALIGARIS ◽  
J. J. ASTRADA ◽  
S. TALEISNIK
Keyword(s):  
Luteinizing Hormone ◽  
Single Injection ◽  
Significant Rise ◽  
Female Rats ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Old Rats ◽  
Lh Secretion ◽  
Phasic Release

SUMMARY In immature female rats serum luteinizing hormone (LH) concentration, as measured by radioimmunoassay, was found to be higher at 10 or 15 days of age than thereafter. Animals ovariectomized soon after birth or at 5 days of age showed a significant rise in serum LH levels 10 days later. A positive feedback effect on LH secretion was observed on the day following a single injection of oestradiol benzoate (OB) in 28-day-old rats but not in younger animals. However, in animals primed with OB a second dose of OB 2 days later resulted in a significant rise in serum LH levels even in rats of 22 days of age. Progesterone (1 mg) injected 3 days after the injection of a single dose of OB induced, a few hours later, a significant rise in serum LH concentration. This effect was observed from the 22nd day of age but not in younger animals. The magnitude of the response to progesterone, as revealed by the serum LH levels, sharply decreased at the time of puberty. It is concluded that the mechanisms responsible for the tonic release of LH are ready to function at the time of birth or shortly thereafter, while those involved in the phasic release mature around 22 days of age.

Sign in / Sign up

Export Citation Format

Share Document