Facilitation or Inhibition of the Oestradiol-Induced Gonadotrophin Surge in the Immature Female Rat by Progesterone: Effects on Pituitary Responsiveness to Gonadotrophin-Releasing Hormone (GnRH), GnRH Self-Priming and Pituitary mRNAs for the Progesterone

2007 ◽  
Vol 19 (12) ◽  
pp. 988-1000 ◽  
Author(s):  
B. Attardi ◽  
R. Scott ◽  
D. Pfaff ◽  
G. Fink
1977 ◽  
Vol 74 (1) ◽  
pp. 11-21 ◽  
Author(s):  
M. WILKINSON ◽  
D. DE ZIEGLER ◽  
DANIELLE CASSARD ◽  
K. B. RUF

The effects of oestrogen priming on the sensitivity of the anterior pituitary gland to stimulation with gonadotrophin releasing hormone (GnRH) was investigated in immature female rats using a new organ culture technique. Hemipituitary glands obtained from animals primed with a single dose of oestradiol benzoate (OB; 20 μg/100 g body weight) released significantly more LH when pulsed with GnRH (4 nmol/l) than did control hemipituitary glands. This potentiating effect was detectable as early as 5 days after birth. After a second stimulation, LH secretion remained high. These results were compared with those obtained from animals treated to induce increased levels of endogenous oestrogen on day 26 of life. Thus, hemipituitary glands were obtained from animals given two injections of OB, an injection of pregnant mare serum gonadotrophin (PMSG) or a unilateral brain lesion placed in the basal hypothalamus. Pituitary tissue was stimulated as before with a pulse of GnRH. Two injections of OB enhanced the sensitivity to stimulation. Conversely, both PMSG and lesion treatment severely reduced the sensitivity to GnRH, although PMSG-treated and lesioned animals have been used as models for the study of ovulation.


1977 ◽  
Vol 74 (1) ◽  
pp. 99-109 ◽  
Author(s):  
D. DE ZIEGLER ◽  
M. WILKINSON ◽  
DANIELLE CASSARD ◽  
K. B. RUF

An investigation of pituitary sensitivity, assessed in terms of increments in plasma LH and FSH concentrations, to stimulation with one or two injections of gonadotrophin releasing hormone (GnRH) was carried out on 26-day-old immature female rats which had received one of the following priming treatments: 10 μg oestradiol benzoate (OB) as a single injection on day 23 or day 25, or on both days; 10 i.u. pregnant mare serum gonadotrophin (PMSG) on day 24; an electrochemical brain lesion placed in the mediobasal hypothalamus on day 23; control animals received either vehicle alone or a sham lesion. Pituitary sensitivity assessed at 10.00 h on day 26, after one or two injections of GnRH (100 ng/100 g body weight, s.c.), was enhanced to a similar degree in the three groups treated with OB in terms of LH (P < 0-01). The FSH response also increased after OB treatment but was not statistically significant. In contrast, 48 h after the injection of PMSG (i.e. when the rats were in a 'pro-oestrous-like' condition) pituitary sensitivity in terms of both LH and FSH dropped sharply (P < 0·001). In lesioned animals, pituitary sensitivity to one injection of GnRH was unchanged. A second GnRH injection administered after a 60 min interval induced a slightly larger LH response in control animals. In contrast, the ratio of the second response to the first increased in animals treated with PMSG, despite the state of overall decrease in sensitivity, being 4·5:1 in PMSG-treated rats versus 1·4:1 in controls. In a second set of experiments, we investigated the variation of pituitary sensitivity in conjunction with an experimentally induced gonadotrophin surge. In animals treated with OB on day 23 and with 1 mg progesterone at 12·00 h on day 26, pituitary sensitivity was increased at both 14.00 and 17.00 h as compared with that in the day 23 OB-treated group at 10.00 h. The PMSG-treated animals maintained their state of decreased responsiveness at 14.00 h, but exhibited increased pituitary sensitivity at the time of the gonadotrophin surge (17.00 h). These results show that OB increases pituitary sensitivity to GnRH in 26-day-old female rats and that the induction of a gonadotrophin surge further increases this sensitivity. In contrast, PMSG-treated rats displayed a state of decreased responsiveness 48 and 52 h, but not 55 h, after the injection. Pituitary sensitivity on the second day after PMSG treatment thus clearly differs from that observed during pro-oestrus in the adult cyclic female rat.


1992 ◽  
Vol 132 (3) ◽  
pp. 395-NP ◽  
Author(s):  
F. Kotsuji ◽  
K. Hosokawa ◽  
T. Tominaga

ABSTRACT Gonadotrophin-releasing hormone (GnRH) has been shown to regulate the synthesis and release of gonadotrophins acutely, yet few studies have investigated the chronic effects of this agent on pituitary gonadotrophins. In the present study we determined the effect of chronic administration of GnRH on the female rat pituitary gland. Rats of 8 weeks of age were injected s.c. with various doses of GnRH daily for 30 days. After completion of the GnRH treatment, treated rats and age-matched controls were killed by decapitation at 09.00 h on the first day of dioestrus, as determined from vaginal smears. Treatment with 10 ng–10 μg GnRH/day increased pituitary contents of FSH and LH in a dose-dependent manner. The change in FSH content was much greater than that of LH content. The pituitary FSH content of rats treated with 40 μg GnRH was significantly less than that of rats treated with 10 μg GnRH. There was a marked increase in the number of cells which stained positively for FSH (266%) and LH (28%) in the anterior pituitary of rats given 10 μg GnRH, but there was no demonstrable change in the areas of single cells stained positively for FSH and LH. Serum levels of LH, FSH and oestradiol were not affected by the GnRH treatment. These data indicate that chronic administration of GnRH is capable of increasing the pituitary gonadotrophin content and numbers of FSH and/or LH-stained cells and that FSH cells are affected more than LH cells by the GnRH treatment. The increase in pituitary gonadotrophin content, however, does not necessarily produce an increase in circulating levels of gonadotrophins. Journal of Endocrinology (1992) 132, 395–400


1991 ◽  
Vol 130 (2) ◽  
pp. 169-175 ◽  
Author(s):  
T. Battmann ◽  
S. Mélik Parsadaniantz ◽  
B. Jeanjean ◽  
B. Kerdelhué

ABSTRACT The effects of substance P (SP) on the preovulatory surge of LH and on the inhibitory and stimulatory effects of oestradiol-17β and progesterone on gonadotrophin-releasing hormone (GnRH)-induced LH release were investigated in vivo and in vitro in the rat. A single s.c. injection of 100 μg SP at 12.00 h on the day of pro-oestrus significantly decreased the preovulatory surge of LH. In vitro, the inhibitory effect of oestradiol-17β on GnRH-induced LH release was not modified by treatment with SP. The stimulatory effect of progesterone on GnRH-induced LH release was reduced by treatment with SP. It is concluded that SP may play a modulatory role in the neuroendocrine control of the preovulatory LH surge. Journal of Endocrinology (1991) 130, 169–175


1984 ◽  
Vol 100 (2) ◽  
pp. 175-182 ◽  
Author(s):  
D. J. S. Sirinathsinghji ◽  
L. Martini

ABSTRACT The roles of dopamine and the endogenous opiate peptides in the mediation of the inverse relationship between prolactin and gonadotrophin secretion during lactation were studied by comparing the effects of bromocriptine and naloxone on plasma levels of prolactin, LH and FSH during suckling in the female rat. The effects of exogenous gonadotrophin releasing hormone (GnRH) on the LH and FSH responses to bromocriptine and naloxone were also assessed. In control animals (saline), there was a marked fall in LH levels and a large increase in prolactin levels within 15 min of suckling. In response to GnRH (25 ng) there was a small progressive increase in LH levels reaching a maximum at 45 min. Both bromocriptine (500 μg) and naloxone (500 μg) markedly suppressed the suckling-induced prolactin surge when administered in two separate groups of animals. However, despite the bromocriptine-induced suppression of prolactin levels, there was no increase in LH levels which remained low throughout the suckling period. Naloxone (500 μg), however, induced a twofold increase in LH levels within 15 min suggesting that an enhanced opiate rather than dopaminergic activity may be responsible for the suppression of GnRH and hence gonadotrophin secretion during suckling. This is supported by the finding that whereas combined bromocriptine (500 μg) and GnRH (25 ng) treatment suppressed the suckling-induced prolactin rise and also induced only a small progressive increase in LH (similar to GnRH alone), combined naloxone (500 μg) and GnRH (25 ng) treatment induced a sharp sixfold increase in LH levels within 15 min while at the same time markedly suppressing prolactin levels. None of these drug treatments affected the levels of FSH. The results of this study may thus indicate that (1) the suckling stimulus itself rather than the high prolactin levels may be responsible for the suppression of gonadotrophin secretion during lactation, (2) although dopamine may be an important physiological factor controlling prolactin secretion, it may not be involved in the regulation of LH during lactation and (3) the suckling stimulus may enhance the release of endogenous opiates within the central nervous system which could then stimulate prolactin and at the same time inhibit gonadotrophin secretion by inhibiting GnRH release. This opiate-mediated mechanism may explain the reciprocal nature of prolactin and LH secretion during lactation. J. Endocr. (1984) 100, 175–182


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