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Ramirez & Sawyer (1965) demonstrated that in female rats in pro-oestrus, a marked drop in the luteinizing hormone-releasing factor (LH-RF) in the stalk median eminence occurs only after the ovulatory release of LH. The authors postulated that the LH released may inhibit the synthesis of LH-RF by a negative feedback action. If this assumption is correct, artificial maintenance of an increased level of LH in the hypothalamus should suppress the postovulatory increase of LH-RF in the stalk median eminence that was observed by the same authors and is probably necessary for the subsequent ovulation. To test this hypothesis, adult female Wistar rats, exposed to light from 05.00 to 19.00 h, and with regular 4-day cycles were used. They were implanted with intrahypothalamic ovine LH (NIH-LH-S 15) or with cholesterol between 09.00 and 12.00 h on the day of oestrus.
The LH implants were prepared by tamping a 1:1 mixture of
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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.
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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.
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Hohlweg (1934) was the first to demonstrate corpus luteum formation in prepubertal female rats after oestrogen injection. This ' Hohlweg effect' was later confirmed by numerous workers. It is prevented by hypophysectomy (Hohlweg & Chamorro, 1937), or trans-section of the hypophysial stalk (Westman & Jacobsohn, 1938). The present study was made to see whether, in rats of the Wistar strain (Rehbrücke), the Hohlweg effect is based on a sex-specific reaction of the hypothalamo-hypophysial system.
Intact prepubertal female rats weighing 40–50 g. were injected s.c. with 12 or 30 μg. oestradiol benzoate (EB) dissolved in 0·2 ml. sesame oil, or with oil alone. Five days later the animals were killed and the uteri and Fallopian tubes removed. The ova were obtained by flushing the uteri with saline and opening the tubes and were counted with the help of a dissecting microscope, the ovaries were fixed in Zenker's solution, sections, 5μ thick, were
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It is now well established that progesterone can both facilitate and inhibit ovulation in the rat. In the adult female rat these responses are dependent on the stage of the oestrous cycle as was shown by Everett (1948) and recently confirmed by Zeilmaker (1966). A hypothalamic site of action for progesterone in the facilitation of ovulation was demonstrated by Barraclough, Yrarrazaval & Hatton (1964). On the other hand, ever since Hohlweg (1934) observed the induction of corpus luteum formation by oestrogen in prepubertal female rats, a close connexion between the preovulatory rise of oestrogen and ovulation-inducing gonadotrophin release was suggested by many investigators, and Döcke & Dörner (1965) concluded that oestrogen may increase the sensitivity of the hypophysis to the stimulating effect of the hypothalamic gonadotrophin-releasing factor(s). The present study was made to see whether a synergism between oestrogen and progesterone in the induction of ovulation can be shown in
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SUMMARY
To study the mechanism of the ovulation-inhibiting effect of chlormadinone acetate, different quantities of this progestogen were implanted into one or both ovaries of dioestrous female rats. Introduction of the subcutaneously effective dose into one ovary suppressed ovulation in both, but implantation of half of this quantity did not influence spontaneous ovulation. On the other hand, 1/100 of the subcutaneously effective dose, implanted into the medio-basal hypothalamus or the anterior pituitary of adult dioestrous female rats, and of prepubertal females simultaneously injected with oestradiol benzoate, inhibited spontaneous and oestrogen-induced ovulations respectively. In juvenile rats the main site of action was the median eminence—anterior pituitary region. Chlormadinone was then implanted into the anterior hypothalamus or the anterior pituitary of adult dioestrous rats, and the median eminence was electrically stimulated during the 'critical period' in pro-oestrus. Since implants in the adenohypophysis prevented ovulation whereas implants in the anterior hypothalamus did not, a hypophysial site of action is suggested. On the basis of these results and of former findings on the action of oestrogens in ovulation, a hypothesis involving a competitive antagonism between oestrogen and progestogen at the hypophysial level is advanced to explain the acute ovulatory effects of these steroids.
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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
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ABSTRACT
Oestrogen priming of the central nervous system is required for the positive feedback of oestrogen, and the sensitivity of the negative feedback of oestrogen can be reduced by oestrogen itself. Using adult female and male rats we examined the possibility that these effects depend upon a common mechanism of oestrogen action that is mediated by the medial preoptic area (MPOA). Guide cannulae were implanted in the MPOA of 4-day cyclic rats which were ovariectomized during the evening of day 1 of dioestrus. Glass capillary tubes containing different substances were placed in the cannulae between 09.00 and 12.00 h on the presumptive day 2 of dioestrus. The effectiveness of oestrogen priming was evaluated by examining whether an s.c. implant of oestradiol-17β (OE2) induced an LH surge, and the inhibitory effect of oestrogen on tonic LH secretion was investigated by injecting the rats with 3 μg oestradiol benzoate (OB)/100 g body weight.
The priming effect of an s.c. implant of OE2 could be imitated by the bilateral implantation in the MPOA of a mixture of OB and cholesterol at a ratio of 1:360 for 3 h only. Similar medial preoptic oestrogen implantation also significantly reduced the LH-inhibiting effect of OB. In accord with findings obtained in former studies on desensitization of the negative oestrogen feedback, oestrogen priming resulting from the s.c. administration of OE2 could be suppressed by short-term medial preoptic implantation of clomiphene citrate or apomorphine; bilateral electrical stimulation of the medial amygdaloid nucleus induced an increase in the serum concentration of LH in ovariectomized females implanted with OB in the MPOA, but not in castrated males pretreated and implanted with OB.
The data are compatible with the hypotheses (1) that desensitization of the negative feedback and priming for the positive feedback of oestrogen depend, at least partly, upon a common mechanism of oestrogen action in rats, (2) that slight increases in the medial preoptic oestrogen concentration on the morning of the day of dioestrus create changes which evoke both completion of maturation of preovulatory follicles and ovulation, and (3) that one object of oestrogen priming may be to facilitate the passage of oestrogen-induced neural stimuli from the medial amygdala to the median eminence.
Journal of Endocrinology (1990) 126, 395–402
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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
