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G. Bolet, M. Meunier, M.R. Blanc, L. Martinet and J.C. Poirier


Mating induces a surge of both LH and FSH in the blood of female rabbits, followed 10–12 h later by a surge of FSH only, which begins at the time of ovulation. We have studied the effect of suppression of ovulation on the post-ovulatory surge of FSH. In the first experiment, follicular fluid and oocytes were withdrawn from the largest follicles 8 h after coitus. In the second experiment, ovulation was inhibited by injecting the rabbits with 25 mg indomethacin/kg body weight 7·5 h after mating. Levels of serum FSH and LH were measured for 24-48 h after mating. Control rabbits ovulated normally in both experiments. The treatments did not significantly affect the levels of serum FSH in either experiment, although the second surge of FSH was slightly higher after fluid had been aspirated from the preovulatory follicles. These observations show that the post-ovulatory surge of serum FSH is not dependent upon the completion of ovulation and that it is programmed before 7·5–8 h post coitum.

J. Endocr. (1987) 112, 57–61

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J. E. Sánchez-Criado, C. Bellido, F. J. López and F. Galiot


Administration of the antiprogesterone RU486 to 4-day cyclic rats from metoestrus to pro-oestrus increases serum levels of LH while decreasing levels of FSH. If it is assumed that there is only one gonado-trophin-releasing hormone, there is no direct explanation for the decrease in FSH concentrations. The purpose of these experiments was to investigate the effect of RU486 on gonadotrophin secretion in cyclic rats during periods when the secretion of LH and FSH diverges. RU486 blunted the transient increase in FSH concentration on the afternoon of metoestrus and the compensatory ovarian hypertrophy on the next day of oestrus in unilaterally ovariectomized 4–day cyclic rats. In addition, bilateral ovariectomy reversed the effect of RU486 on the basal secretion of FSH. RU486 induced an increase in basal LH concentrations. Since ovarian inhibin decreases the basal release of FSH, and decreases in peripheral inhibin seem to be responsible for the transient rise in FSH during the oestrous cycle, the effect of RU486 on serum levels of LH and FSH during dioestrus in rats injected with a sheep anti-inhibin serum (AIS) were further evaluated. Treatment with AIS increased FSH levels in oil-treated rats without altering the levels of LH. In contrast, the effects of AIS on FSH secretion were blunted in RU486-treated rats. The results suggest that inhibin might be involved in the RU486-induced decrease of FSH secretion in cyclic rats.

Journal of Endocrinology (1992) 134, 43–49

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J. L. Vandalem, M. McNamara, R. Petit and G. Hennen


Changes in the concentrations of LH and FSH testicular receptors have been studied in the pig, from neonatal to adult life, and correlated with blood LH, FSH and testosterone concentrations.

Quantification of gonadotrophin receptors was performed in equilibrium binding studies, using homologous systems. The presence of high-affinity binding sites for LH and FSH (association constant (K a): LH ∼ 20 litres/nmol; FSH ∼ 10 litres/nmol) was demonstrated in the testes of all animals studied. The apparent affinity of LH and FSH receptors did not change significantly with age.

During the first weeks of life, there was a transient rise in LH receptor content, reaching a maximum of 8·7 ± 2·2 (mean ± s.e.m.) pmol/g testis at 24 days of age. This was correlated with a peak in testosterone secretion and reflects the second wave of interstitial cell proliferation in the pig. A second increase in the number of LH receptors occurred after 12 weeks of age and corresponds to pubertal maturation and final differentiation of adult Leydig cells. During this period, circulating concentrations of testosterone markedly increased without any significant variation in LH blood levels, suggesting a change in testicular sensitivity to LH in the maturing pig.

A continuous increase in FSH receptor content was observed from the neonatal to the adult pig. This increase occurred in two phases. During the first 2 months of life, the increase in the number of FSH receptors exceeded that of testis growth rate and resulted in an increase in FSH receptor concentrations which reached a peak at 12·1 ± 1·8 pmol/g testis, at week 9. After this time the increase in the amount of FSH receptors was slower than that of testis weight gain, leading to a decrease in receptor concentration.

Since changes in the amounts of LH and FSH receptor concentrations were not correlated with variations in gonadotrophin concentrations in the blood, an inductive role for FSH on LH receptors, as has been shown in the rat, could thus not be demonstrated in the pig.

J. Endocr. (1986) 111, 301–308

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M Kanzaki, M-A Hattori, R Horiuchi and I Kojima


The actions of FSH and Insulin-like growth factor-I (IGF-I) were studied in cultured rat ovarian granulosa cells. Cells became differentiated and expressed LH receptors when they were incubated for 72 h with 200 μg FSH/l (high FSH) but not 20 μg FSH/l (low FSH). Treatment with high but not low FSH increased the release of both immunoreactive and bioactive IGF-I into the medium. A combination of low FSH and IGF-I reproduced the effect of high FSH on LH receptor expression. We then examined the critical time when low FSH and IGF-I exerted their effects. In the presence of continuous low FSH, IGF-I was capable of inducing LH receptor expression even when added 24 h after the addition of low FSH. However, when IGF-I was added at 36 h, LH receptor expression measured at 72 h was greatly reduced. In contrast to the action of IGF-I, continuous exposure to low FSH was required for LH receptor expression, and IGF-I had no effect when FSH was not included for the entire 72 h of culture.

DNA synthesis as assessed by both [3H]thymidine incorporation and nuclear bromodeoxyuridine labelling was moderate at the beginning of culture and markedly reduced at 24 h both in the presence and absence of either high FSH or low FSH plus IGF-I. In the presence of either high FSH or a combination of low FSH plus IGF-I, DNA synthesis remained decreased for up to 72 h whereas it began to increase in the absence of either high FSH or a combination of low FSH plus IGF-I. A similar increase in DNA synthesis was observed after 48 h when granulosa cells were treated with low FSH alone, which did not induce LH receptor expression. These results indicate that 1) growth and differentiation of granulosa cells are regulated inversely; 2) FSH and IGF-I act together to induce LH receptor expression; and 3) action of IGF-I is dependent on the presence of FSH.

Journal of Endocrinology (1994) 141, 301–308

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Faculty of Agriculture, Nagoya University, Nagoya 464, Japan

(Received 6 July 1976)

In 1965, Shinde, Ôta & Yokoyama reported that the initiation of lactose synthesis in the mammary gland could be advanced by ovariectomy and/or foeto-placentectomy performed on days 18 or 19 of pregnancy in the rat. The present experiments were designed to determine the stage of pregnancy at which the mammary gland was able to initiate lactose synthesis in response to ovariectomy. Corticosterone in plasma was also measured in relation to the changes around the time of lactogenesis reported previously (Ôta, Ôta & Yokoyama, 1974).

Primigravid Wistar-Imamichi strain rats, weighing between 200 and 280 g, were kept in a temperature- (23 ± 2°C) and light- (14h light: 10h darkness, lights on 05.00h) controlled animal room. The day on which sperm in the vagina or vaginal plugs were found was designated day 0 of pregnancy. Ovariectomy was performed between 17.30 and 18.00

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When 1·0 μg luteinizing hormone releasing hormone (LH-RH) was given i.v. three times at 1 h intervals from 17.00 to 19.00 h on the day of dioestrus (day 0) to regular 4 day cyclic rats, premature ovulation was induced the next morning (day 1) with the number of ova present comparable to normal spontaneous ovulation. The next spontaneous ovulation occurred on the morning of day 5, 4 days after premature ovulation induced by LH-RH.

Plasma concentrations of FSH and LH showed transient rises and falls within 1 h of administration of LH-RH; concentrations of FSH in the plasma decreased from 20.00 h on day 0 but markedly increased again from 23.00 h on day 0 to 02.00 h on day 1 and these high levels persisted until 14.00 h on day 1, with only a small increase of plasma LH during this period. The duration of increased FSH release during premature ovulation induced by LH-RH treatment was 6 h longer than the FSH surge occurring after administration of HCG on day 0. Surges of gonadotrophin were absent on the afternoon of day 1 (the expected day of pro-oestrus) and the surges characteristic of pro-oestrus occurred on the afternoon of day 4 and ovulation followed the next morning. The pituitary content of FSH did not decrease despite persisting high plasma levels of FSH during premature ovulation induced by either LH-RH or HCG on day 0.

The changes in uterine weight indicated that the pattern of oestrogen secretion from the day of premature ovulation induced by LH-RH to the day of the next spontaneous ovulation was similar to that of the normal 4 day oestrous cycle. When 10 i.u. HCG were given on day 0, an increase in oestrogen secretion occurred on day 2, 1 day earlier than in the group given LH-RH on day 0. This advancement of oestrogen secretion was assumed to be responsible for the gonadotrophin surges on day 3.

Similar numbers of fully developed follicles were found by 17.00 h on day 2 after premature ovulation induced by either LH-RH or HCG, suggesting that the shorter surge of FSH during premature ovulation induced by HCG had no serious consequences on the initiation of follicular maturation for the succeeding oestrous cycle in these rats.

Administration of LH-RH on day 0 had no direct effect on the FSH surge during premature ovulation. Secretory changes in the ovary during ovulation may be responsible for this prolonged selective release of FSH.

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Section of the mammary nerves in goats and sheep or complete section of the spinal cord in the rabbit, rat, goat and cat (see review by Denamur, 1965) results in the suppression of suckling-induced milk ejection. In lactating women, Theobald (1959) failed to interrupt milk ejection by anaesthesia of the nipples produced by infiltration with 15 ml. of 1% lignocaine, but conditioning of oxytocin release to non-mammary stimuli may have occurred in these cases.

In the present experiments the milk-ejection reflex was tested in six multiparous rabbits of mixed breed by the method of Cross & Harris (1952), in which litter weight gain during suckling is taken as an indicator of oxytocin release. The rabbits were separated from their litters on the day after parturition and daily suckling tests began at 10.00 hr. on the following day. A variety of treatments were applied before nursing. The teats were anaesthetized by

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J. J. Evans, G. Robinson and K. J. Catt


Neurohypophysial hormones have been implicated in the control of anterior pituitary function, and oxytocin has been shown to stimulate gonadotrophin excretion and ovarian follicular development in certain species. To determine the role of neurohypophysial peptides in the control of gonadotrophin release, their actions on LH and FSH secretion were analysed in rats in vivo and in vitro. In adult female rats, administration of oxytocin during early pro-oestrus advanced the spontaneous LH surge and markedly increased peripheral LH levels at 15.00 h compared with control animals. In cultured pituitary cells from adult female rats, oxytocin and vasopressin elicited dose-related increases in LH and FSH release. Such responses were not affected by a potent gonadotrophin-releasing hormone (GnRH) antagonist that abolished GnRH agonist-induced release of LH and FSH. Oxytocin did not enhance GnRH agonist-stimulated gonadotrophin release to the same extent as it increased basal secretion, but at low concentrations of GnRH agonist the effects were additive. The gonadotrophin responses to oxytocin and vasopressin were inhibited by the specific neurohypophysial hormone antagonists, [d(CH2)5 d-Ile2,Ile4,Arg8]vasopressin and [d(CH2)5Tyr (Me),Arg8]vasopressin. These results provide direct evidence that neurohypophysial hormones can stimulate gonadotrophin secretion through a receptor system distinct from the GnRH receptor. Such a mechanism could represent a complementary hypothalamic control system for long-term modulation of LH and FSH secretion by exerting a basal or tonic influence on gonadotrophin production.

Journal of Endocrinology (1989) 122, 99–106

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A. N. Corps and K. D. Brown


Samples of human and ruminant mammary secretions stimulated the proliferation of rat intestinal epithelial (RIE-1) cells in culture. The stimulation was dose-dependent, and samples taken prepartum had greater potency than those taken after parturition. When various hormones and growth factors known to be present in milk were tested, only epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I) stimulated the proliferation of RIE-1 cells. IGF-I was effective at lower concentrations than insulin, and the maximal stimulation induced by each of these two polypeptides was greater than that induced by EGF. The maximal stimulation induced by samples of mammary secretions was similar to that induced by insulin or IGF-I.

J. Endocr. (1987) 113, 285–290

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Laboratoire de Physiologie des Poissons and *Laboratoire de Physiologie de la Lactation, I.N.R.A., 78350 Jouy en Josas, France

(Received 11 October 1976)

Fish prolactin bioassays lack specificity (Sage & Bern, 1972), have poor sensitivity, are difficult to use (Ensor & Ball, 1968; Clarke, 1973) and contradictory conclusions have been drawn with them. Nicoll & Bern (1968) obtained no lactogenic effect of teleost pituitary gland in the pigeon-crop and the rabbit mammary gland tests, but Chadwick (1966) demonstrated the occurrence of a mammotrophic effect. Other workers have used heterologous radioimmunoassay (RIA) systems (McKeown & Van Overbeeke, 1972); these RIA systems do not seem to cross-react specifically with fish prolactin (Nicoll, 1975). We present a new approach using rabbit mammary gland prolactin receptors.

The technique used was a modification of the radioreceptor assay (RRA) for lactogenic hormones (Shiu, Kelly & Friesen, 1973). At the beginning of lactation the rabbit was injected with