DEVELOPMENT OF THE MECHANISMS INVOLVED IN THE FACILITATORY AND INHIBITORY EFFECTS OF OVARIAN STEROIDS ON THE RELEASE OF FOLLICLE-STIMULATING HORMONE IN THE IMMATURE RAT

1973 ◽  
Vol 58 (3) ◽  
pp. 547-554 ◽  
Author(s):  
L. CALIGARIS ◽  
J. J. ASTRADA ◽  
S. TALEISNIK

SUMMARY Serum follicle-stimulating hormone (FSH) concentration was found to be higher in neonatal female rats than in adults. The values increased to a maximum on day 15 and decreased thereafter. Ovariectomy soon after birth or at 5 days of age induced a significant rise in serum FSH concentration 9 days later. Administration of 10 μg oestradiol benzoate (OB) lowered FSH concentration in both intact and spayed animals. Progesterone (1 mg) injected 3 days after priming female rats with a single dose of 10 μg OB induced, on the same day, a significant rise in serum FSH concentration in animals older than 22 days of age. In younger animals progesterone reversed the effect of OB. The facilitatory effect of progesterone occurred when the hormone was given in the afternoon but not when it was given in the morning. Male rats, although showing the negative feedback effect of OB injection, failed to show the positive feedback effect of progesterone. It is concluded that the central nervous system—hypophysial mechanism responsible for FSH secretion is ready to function before puberty. In female rats initiation of puberty probably depends on the activation of that mechanism by appropriate facilitatory ovarian steroid signals.

1963 ◽  
Vol 26 (3) ◽  
pp. 425-436 ◽  
Author(s):  
P. S. BROWN

SUMMARY A dithiocarbamoylhydrazine (ICI 33828) was injected s.c. into intact rats and mice. It usually caused a reduction in weight of the uterus or of the accessory organs in the male, but less commonly of the gonads. As little as 0·5 mg. daily for 4 days caused significant effects in adult female rats, while half this dose on alternate days retarded maturation in male rats. ICI 33828 was injected with exogenous gonadotrophin in three systems of assay and in some cases it modified the response to the gonadotrophin. This may not be due to a specific effect at the gonadal level but either to suppression of endogenous gonadotrophins in the test animals or to the effect of ICI 33828 on their general condition. Pituitary glands from male rats treated with ICI 33828 were assayed for follicle stimulating hormone (FSH) and found to contain significantly less than glands from control rats. This suggests that ICI 33828 acts by reducing the formation of pituitary gonadotrophin.


1977 ◽  
Vol 74 (1) ◽  
pp. 143-144 ◽  
Author(s):  
J. A. MOGUILEVSKY ◽  
P. SCACCHI ◽  
L. RUBINSTEIN

Department of Neuroendocrinology, Centro de Investigaciones Médicas Albert Einstein (CIMAE), Luis Viale 2831, Buenos Aires, Argentina and *Department of Obstetrics and Gynecology, UCLA School of Medicine, Los Angeles, California, U.S.A. (Received 18 January 1977) It is generally accepted that the administration of androgens to female rats in the neonatal period suppresses cyclic gonadotrophin release and a tonic gonadotrophin release occurs (Barraclough, 1966; Gorski, 1971). The tonic or male gonadotrophin pattern characteristically shows higher levels of plasma and pituitary follicle-stimulating hormone (FSH) and serum prolactin compared with female rats (Johnson, 1967, 1971; Kragt & Ganong, 1968; Neill, 1972). In spite of the fact that the neonatal administration of androgens also induces changes in the reproductive physiology of adult male rats (Johnson & Witscht, 1963; Johnson, Yasuda & Sridharan, 1964; Morrison & Johnson, 1966), the effect of androgenization on gonadotrophin secretion in this sex is not clear. The purpose of the present study


1991 ◽  
Vol 125 (3) ◽  
pp. 280-285 ◽  
Author(s):  
J. Alan Talbot ◽  
Ann Lambert ◽  
Robert Mitchell ◽  
Marek Grabinski ◽  
David C. Anderson ◽  
...  

Abstract We have investigated the role of Ca2+ in the control of FSH-induced estradiol secretion by Sertoli cells isolated from 8-10 days old rats. Exogenous Ca2+ (4-8 mmol/1) inhibited FSH-stimulated E2 secretion such that, with 8 mmol/l Ca2+ and FSH (8 IU/l) E2 secretion decreased from 2091±322 to 1480±84 pmol/l (p<0.002), whilst chelation of Ca2+ in the culture medium with EGTA (3 mmol/l) increased E2 secretion from 360±45 to 1242±133 pmol/l) in the absence of FSH. Further, EGTA (3 mmol/l) markedly potentiated FSH (8 IU/l), forskolin (1 μmol/l) and dibutyryl cAMP (1 mmol/l)-stimulated E2 secretion. Addition of the Ca2+ ionophores, ionomycin (2-5 μmol/l) and A23187 (2 μmol/l), inhibited FSH (8 IU/l)-stimulated E2 secretion by >80%. The effect of ionomycin was totally reversible, whereas that of A23187 was irreversible. Ionomycin (5 μmol/l) had no effect on EGTA-induced E2 secretion in the absence of FSH, but reduced EGTA-provoked E2 secretion by 59% in the presence of FSH (8 IU/l). Similarly, forskolin- and dibutyryl cAMP-provoked E2 production was inhibited 46-50% by ionomycin (5 μmol/l). We conclude that FSH-induced E2 secretion from immature rat Sertoli cells is modulated by intra- and extracellular Ca2+.


Life Sciences ◽  
1985 ◽  
Vol 36 (9) ◽  
pp. 889-899 ◽  
Author(s):  
Henry M. Jones ◽  
Constance L. Wood ◽  
Michael E. Rush

1972 ◽  
Vol 50 (8) ◽  
pp. 768-773 ◽  
Author(s):  
E. A. Ibrahim ◽  
B. E. Howland

The concentration of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in serum and pituitary glands was studied in intact female rats and rats that were ovariectomized on day 0 of the experiment and then starved or fed for 2, 4, 7, or 9 days. Ovariectomy resulted in enhanced rates of synthesis and release of FSH and LH as indicated by the significant (P < 0.01) rises in the concentration of both hormones in the pituitary gland and serum.Starvation resulted in a decrease in body and pituitary weight. The concentration of FSH and LH in pituitary glands of starved rats was higher (P < 0.05) than that in fed rats on days 7 and 9. The concentration of FSH and LH in serum of starved rats was increased after ovariectomy but the levels on days 7 and 9 were lower than those of fed rats.These results suggest that the synthesis of FSH and LH was enhanced in both starved and fed rats following ovariectomy while the rate of release of both hormones was decreased at 7 and 9 days of starvation in comparison with rats fed ad libitum.


1995 ◽  
Vol 132 (3) ◽  
pp. 357-362 ◽  
Author(s):  
M Tena-Sempere ◽  
L Pinilla ◽  
E Aguilar

Tena-Sempere M, Pinilla L, Aguilar E. Orchidectomy selectively increases follicle-stimulating hormone secretion in gonadotropin-releasing hormone agonist-treated male rats. Eur J Endocrinol 1995;132: 357–62. ISSN 0804–4643 The pituitary component of the feedback mechanisms exerted by testicular factors on gonadotropin secretion was analyzed in adult male rats treated with a potent gonadotropin-releasing hormone (GnRH) antagonist. In order to discriminate between androgens and testicular peptides, groups of males were orchidectomized (to eliminate androgens and non-androgenic testicular factors) or injected with ethylene dimethane sulfonate (EDS), a selective toxin for Leydig cells (to eliminate selectively androgens) and treated for 15 days with vehicle or the GnRH antagonist Ac-d-pClPhe-d-pClPhe-d-TrpSer-Tyr-d-Arg-Leu-Arg-Pro-d-Ala-NH2CH3COOH (Org.30276, 5 mg/kg/72 hours). Serum concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured 7 and 14 days after the beginning of treatment. We found that: in males treated with GnRH antagonist, orchidectomy or EDS treatment did not induce any increase in LH secretion; and orchidectomy, but not EDS treatment, increased FSH secretion in GnRH-treated males. The present results show that negative feedback of testicular factors on LH secretion is mediated completely through changes in GnRH actions. In contrast, a part of the inhibitory action of the testis on FSH secretion is exerted directly at the pituitary level. It can be hypothesized that non-Leydig cell testicular factor(s) inputs at different levels of the hypothalamic–pituitary axis in controlling LH and FSH secretion. Manuel Tena-Sempere, Department of Physiology, Faculty of Medicine, University of Córdoba, 14004 Córdoba, Spain


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