Selective release of FSH in lactating rats during the period of follicular atresia induced by the administration of antiserum to LH-releasing hormone

1988 ◽  
Vol 118 (3) ◽  
pp. 455-464 ◽  
Author(s):  
K. Taya ◽  
S. Sasamoto

ABSTRACT Passive immunoneutralization of LHRH by injecting a caprine antiserum to LHRH (LHRH-AS) in lactating rats nursing two pups on day 5 of lactation resulted in an immediate decline in concentrations of LH in the plasma during the 24-h study period, followed by a gradual increase to control levels 30 h later. Concentrations of oestradiol-17β and inhibin activity in ovarian venous plasma also decreased abruptly in LHRH-AS treated animals and recovered to control levels 36 h later. These changes were correlated with changes in concentrations of LH in the plasma. On the other hand, plasma concentrations of FSH increased abruptly in the LHRH-AS treated animals within 3 h after injection, but the concentrations declined gradually to control levels 48 h later. The ability of follicles to ovulate in response to human chorionic gonadotrophin (hCG) began to decrease within 6 h after treatment with LHRH-AS, and further decreased until 18 h after injection of LHRH-AS, when hCG induced ovulation (with two oocytes) in only one of five animals. A gradual increase in ovulation rate to control levels was noted by 36 h after injection of LHRH-AS. These results indicate that Graafian follicles present at the time of LHRH-AS injection had become atretic and that a new set of follicles had then begun to mature. Selective release of FSH could not be induced by injection of LHRH-AS in ovariectomized animals. Treatment with inhibin (porcine follicular fluid) suppressed the selective release of FSH, whereas treatment with oestradiol-17β had no inhibitory effect on the selective release of FSH. These findings indicate (1) that tonic secretion of LH is an important factor in normal follicular maturation and maintenance in lactating rats, (2) that selective release of FSH after injection of LHRH-AS is attributed to the removal of a negative influence of inhibin from antral follicles during the period of follicular atresia and (3) that a selective surge of FSH is responsible for initiation of new follicular maturation. J. Endocr. (1988) 118, 455–464

1988 ◽  
Vol 116 (1) ◽  
pp. 115-122 ◽  
Author(s):  
K. Taya ◽  
S. Sasamoto

ABSTRACT To determine whether failure of follicular maturation during the early stages of lactation in rats is due to inadequate LH stimulation, lactating rats nursing eight pups were injected twice daily for 1–3 days (days 2–5 of lactation) with various doses of ovine LH. Follicular maturation was determined by the ability of the follicles to ovulate in response to 10 IU human chorionic gonadotrophin (hCG), endogenous oestradiol-17β and inhibin production. Ovulation was not induced in control animals in response to 10 IU hCG given between days 2 and 5 of lactation. On the other hand, an injection of 10 IU hCG could induce ovulation in LH-treated animals, in which 25 and 50 μg LH per injection were given s.c. from days 2 to 5 of lactation. Concentrations of oestradiol-17β and inhibin activity in ovarian venous plasma increased progressively after the administration of LH, indicating that induced development of ovulatory follicles had occurred. Plasma concentrations of FSH declined in LH-treated animals compared with those in control animals. The decrease in plasma concentrations of FSH was not observed when lactating rats were ovariectomized before the first injection of LH, indicating that ovarian products, probably inhibin, from developing follicles may suppress the secretion of FSH from the pituitary gland. In both LH-treated and control animals, concentrations of prolactin and progesterone remained increased during the period of LH administration. The present results, therefore, suggest that the plasma levels of LH are an important determinant of follicular maturation during lactation in rats. J. Endocr. (1988) 116, 115–122


1995 ◽  
Vol 146 (1) ◽  
pp. 169-176 ◽  
Author(s):  
H Kishi ◽  
K Taya ◽  
G Watanabe ◽  
S Sasamoto

Abstract Plasma and ovarian levels of inhibin were determined by a radioimmunoassay (RIA) at 3-h intervals throughout the 4-day oestrous cycle of hamsters. Plasma concentrations of FSH, LH, progesterone, testosterone and oestradiol-17β were also determined by RIAs. In addition, hamsters were injected at various times with human chorionic gonadotrophin (hCG) to determine the follicular development. The changes in plasma concentrations of FSH after injection of antisera to oestradiol-17β (oestradiol-AS) and inhibin (inhibin-AS) on the morning of day 2 (day 1=day of ovulation) were also determined. Plasma concentrations of inhibin showed a marked increase on the afternoon of day 1, remained at plateau levels until the morning of day 4, then increased abruptly on the afternoon of day 4 when preovulatory LH and FSH surges were initiated. A marked decrease in plasma concentrations of inhibin occurred during the process of ovulation after the preovulatory gonadotrophin surges. An inverse relationship between plasma levels of FSH and inhibin was observed when the secondary surge of FSH was in progress during the periovulatory period. Plasma concentrations of oestradiol-17β showed three increase phases and these changes differed from those of inhibin. Changes in plasma concentrations of oestradiol-17β correlated well with the maturation and regression of large antral follicles. Follicles capable of ovulating following hCG administration were first noted at 2300 h on day 1. The number of follicles capable of ovulating reached a maximum on the morning of day 3 (24·8± 0·6), and decreased by 0500 h on day 4 (15·0 ± 1·1), corresponding to the number of normal spontaneous ovulations. Plasma concentrations of FSH were dramatically increased within 6 h after inhibin-AS, though no increase in FSH levels was observed after oestradiol-AS. These findings suggest that changes in the plasma levels of inhibin during the oestrous cycle provide a precise indicator of follicular recruitment, and that the changes in plasma concentrations of oestradiol-17β are associated with follicular maturation. These findings also suggest that inhibin may play a major role in the inhibition of FSH secretion during the oestrous cycle of the hamster. Journal of Endocrinology (1995) 146, 169–176


1980 ◽  
Vol 87 (3) ◽  
pp. 393-400 ◽  
Author(s):  
KAZUYOSHI TAYA ◽  
SHUJI SASAMOTO

In order to elucidate the mechanism of the resumption of follicular activity and ovulation in rats, levels of FSH, LH and prolactin in plasma and pituitary gland and ovarian follicular development were quantified after removal of the litter on day 3 of lactation (day of parturition = day 0 of lactation). Such removal resulted in ovulation of 13 oocytes 4 days later, a number comparable with that found in normal cyclic rats. Plasma levels of prolactin were high during lactation but markedly decreased after removal of the litter. Although plasma concentrations of FSH and LH did not change during days 3–7 of lactation, there was an FSH surge between 24 and 30 h after removal of the litter. Plasma concentrations of LH also increased slightly but significantly by 24 h after removal of the litter and this value persisted during the following 2 days. Surges of FSH, LH and prolactin occurred at 17.00 h 3 days after pups were removed. Removal of the litter did not increase pituitary contents of FSH, LH and prolactin and a marked reduction in pituitary levels of FSH and LH, but not of prolactin, occurred at 17 00 h 3 days after removal of the litter. A quantitative study of follicular development indicated that follicles larger than 401 μm in diameter were absent during days 3–7 of lactation. However, the number and size of antral follicles increased by 30 h after removal of the litter, probably due to the increases in plasma levels of FSH and LH, and follicles larger than 601 μm in diameter appeared 3 days after the young were removed. Although ovulation could not be induced by human chorionic gonadotrophin from days 3 to 5 of lactation, its administration 30 h after removal of the litter produced ovulation in all rats by the following morning. These results indicated that a moderate increase in FSH, although below the amounts released at the preovulatory surge, together with basal levels of LH which were within the range observed on the day of dioestrus during the normal cycle were responsible for the initiation of follicular maturation after removal of the litter.


1991 ◽  
Vol 57 (1) ◽  
pp. 41-49 ◽  
Author(s):  
J. L. Spearow ◽  
R. P. Erickson ◽  
T. Edwards ◽  
L. Herbon

SummaryWe have examined the effects of major histocompatibility (H-2) haplotypes and genetic background (all loci other than the H-2 region) on hormone-induced ovulation rate in congenic strains of mice. In comparison with the H-2a haplotype, the H-2b haplotype increased hormone-induced ovulation rate 92% on the A/J (A) genetic background. However, H-2 haplotype did not affect hormone-induced ovulation rate on the C57BL/10J (C57) genetic background. The H-2b-linked gene(s) increased hormone-induced ovulation rate on the A/J genetic background largely by (1) enhancing the maturation of follicles in response to pregnant mare's serum gonadotrophin (PMSG) and (2) altering the stages of follicular development which can be induced to ovulate in response to human chorionic gonadotrophin (hCG). The observed effects of H-2 on hormone-induced ovulation rate were not explained by differences in the timing of puberty, the number of follicles present in untreated females, or the incidence of follicular atresia. The effect of genetic background on hormone-induced ovulation rate was much greater than was the effect of the H-2 region. We found that hormone-induced ovulation rate was five- to six-fold higher on the C57 genetic background than on the A genetic background. The C57 genetic background increased hormone-induced ovulation rate by (1) enhancing the induction of follicular maturation in response to gonadotropins and (2) by reducing the incidence of follicular atresia.


1986 ◽  
Vol 110 (2) ◽  
pp. 279-285 ◽  
Author(s):  
N. Matsuzono ◽  
K. Taya ◽  
G. Watanabe ◽  
S. Sasamoto

ABSTRACT The relationship between a surge of FSH and the initiation of follicular maturation was examined using rats with a 4-day oestrous cycle. When antiserum against LH-releasing hormone (LHRH-AS) was given at 13.00 h on the day of pro-oestrus (day 0), surges of FSH and LH were blocked. Plasma FSH and LH were maintained at low basal levels without a surge release until the next spontaneous surge occurred on the afternoon of day 4, the predicted day of pro-oestrus. Follicular responsiveness to an injection of human chorionic gonadotrophin (hCG) indicated that preovulatory follicles, present at the time of treatment with LHRH-AS, were capable of ovulating on day 1 but had regressed by day 2. Subsequently, as shown by the ovulatory response to hCG, a new set of follicles had begun to mature by the morning of day 3 without a preceding surge of FSH. Changes in oestradiol-17β levels in the plasma throughout the oestrous cycle were the same in rats injected with LHRH-AS or non-immune control serum. The mature follicles in the rats treated with LHRH-AS thus retained the capacity to ovulate after losing their ability to secrete oestrogen. These results suggest that an FSH surge is not essential for initiation of follicular maturation and that basal levels of FSH may be enough to initiate follicular maturation in the absence of newly formed corpora lutea. J. Endocr. (1986) 110, 279–285


1997 ◽  
Vol 152 (1) ◽  
pp. 147-154 ◽  
Author(s):  
A Tohei ◽  
M Akai ◽  
T Tomabechi ◽  
M Mamada ◽  
K Taya

Abstract The functional relationship between thyroid, adrenal and gonadal hormones was investigated using adult male rats. Hypothyroidism was produced by the administration of 4-methyl-2-thiouracil (thiouracil) in the drinking water for 2 weeks. Plasma concentrations of TSH dramatically increased, whereas plasma concentrations of tri-iodothyronine and thyroxine decreased in thiouracil-treated rats as compared with euthyroid rats. Hypothyroidism increased basal levels of plasma ACTH and pituitary content of ACTH. The pituitary responsiveness to CRH for ACTH release markedly increased, whereas the adrenal responsiveness to ACTH for corticosterone release decreased. These results indicated that hypothyroidism causes adrenal dysfunction in adult male rats. Pituitary contents of LH and prolactin decreased in hypothyroid rats as compared with euthyroid rats. In addition, hypothyroidism lowered pituitary LH responsiveness to LHRH. Testicular responsiveness to human chorionic gonadotrophin for testosterone release, however, was not different between euthyroid and hypothyroid animals. These results indicated that hypothyroidism causes adrenal dysfunction and results in hypersecretion of ACTH from the pituitary gland. Adrenal dysfunction may contribute to the inhibition of LHRH secretion from the hypothalamus, possibly mediated by excess CRH. Journal of Endocrinology (1997) 152, 147–154


1982 ◽  
Vol 93 (2) ◽  
pp. 247-NP ◽  
Author(s):  
H. M. Charlton ◽  
Dilys Parry ◽  
D. M. G. Halpin ◽  
R. Webb

Hypogonadal mice are deficient in LH releasing hormone (LH-RH), the releasing factor for LH and FSH, with a consequent failure of postnatal ovarian and testicular development. After intravenous injection of hypogonadal females with 125I-labelled human chorionic gonadotrophin (hCG), followed by autoradiography of semi-thin (1 μm) slices of the ovary, labelled hCG was found to be associated with interstitial cells and thecal cells with little or no labelling of granulosa cells. Labelled human FSH was associated solely with granulosa cells. Hypogonadal females, implanted for 5 days with a silicone elastomer capsule of oestrogen, showed a similar response to that of normal females with hCG labelling of the granulosa cells of the larger follicles as well as of the thecal cell layer. Furthermore, subcutaneous injection of hypogonadal females with LH-RH (50 ng), 12 times daily for 5 days, increased uterine weight and stimulated ovarian development with some large follicles binding hCG to both thecal and granulosa cells. Therefore stimulation of follicular development may possibly be associated with increased oestradiol concentrations. In the male, after injection of 125I-labelled hCG, silver grains were associated with the interstitial cells alone in both hypogonadal and normal mice. Labelled human FSH was undetectable in semi-thin testicular sections, but the mode of injection (intravenous) may not have allowed enough labelled hormone to reach the testis in order to resolve the question as to whether the hypogonadal or normal testis can bind FSH.


1973 ◽  
Vol 72 (3) ◽  
pp. 615-624 ◽  
Author(s):  
W. Maurer ◽  
U. Volkwein ◽  
J. Tamm

ABSTRACT HCG was infused intravenously into normal male subjects. The doses administered were 500, 100 and 50 IU, respectively. During the initial phase of the infusions the plasma testosterone (T) levels decreased. Thirty minutes after starting the infusion of 500 and 100 IU HCG, respectively, the plasma testosterone increased. Significantly elevated values were observed 60 to 180 minutes after the cessation of HCG administration. The dihydrotestosterone (DHT) concentrations in the plasma showed a varying pattern. On the average this steroid also exhibited an increase in plasma following the HCG administration. From the results no conclusions can be drawn as to the extent to which the plasma concentrations of DHT have been influenced by a secretion from the testes or by a peripheral conversion of T into DHT.


1973 ◽  
Vol 57 (1) ◽  
pp. 123-134 ◽  
Author(s):  
E. NIESCHLAG ◽  
D. L. LORIAUX ◽  
H. J. RUDER ◽  
I. R. ZUCKER ◽  
M. A. KIRSCHNER ◽  
...  

SUMMARY The secretion of dehydroepiandrosterone (DHA) and its sulphate (DHAS) was examined by measuring their concentrations in adrenal venous, gonadal venous, and peripheral venous plasma. Both steroids were secreted by the adrenal cortex and the rate of DHA secretion was higher than that of DHAS in seven out of eight subjects. Adrenocorticotrophin (ACTH) caused an increase in DHA and DHAS secretion by 15–30 min after administration. When ACTH was infused for 8 h, peripheral DHA concentrations increased at 2 h and decreased subsequently in five out of eight subjects suggesting depletion of substrate or cofactors for this biosynthetic pathway. Gonadal secretion of DHA was present in each subject (eight women and two men) but DHAS secretion could not be demonstrated. Exogenous human chorionic gonadotrophin (HCG) caused an increase in plasma DHA. Examination of the diurnal variation of plasma DHA concentrations revealed a 40% decrease from 08.00 to 20.00 h.


1985 ◽  
Vol 106 (1) ◽  
pp. 31-NP ◽  
Author(s):  
G. Watanabe ◽  
K. Taya ◽  
S. Sasamoto

ABSTRACT The present study was undertaken to determine whether hypothalamic differentiation is involved in the selective release of FSH during the periovulatory period using adult male rats castrated and implanted with an ovary. Adult male rats (70–90 days old) were castrated and an ovary obtained from a prepubertal female rat (26 days old) was immediately grafted subcutaneously. Four weeks later, human chorionic gonadotrophin (hCG, 10 i.u.) was injected i.v. into the experimentally manipulated rats to induce ovulatory changes in the grafted ovaries. Another group of similarly prepared rats was injected with 0·9% (w/v) NaCl solution as controls. After injection of hCG, plasma concentrations of FSH increased significantly by 6 h, reached peak values at 12 h and declined to control levels at 36 h. On the other hand, plasma concentrations of LH were reduced by 6 h and decreased further during the next 36 h. An abrupt fall in plasma concentrations of oestradiol-17β occurred within 3 h of the administration of hCG. Histological examination revealed that ovulatory changes and luteinization of follicles were induced in grafted ovaries by 18 h after the injection of hCG. Thirty-six hours after treatment with hCG, a set of newly formed corpora lutea was observed in grafted ovaries and plasma concentrations of progesterone were raised. Treatment with oestradiol-17β did not inhibit the selective release of FSH after the administration of hCG, suggesting that the abrupt decrease in secretion of oestradiol-17β from the grafted ovary is not involved in the occurrence of the FSH surge. These results indicate that a selective release of FSH can be induced in castrated male rats bearing an ovarian transplant probably due to decreased secretion of inhibin by the luteinized follicles in the grafted ovaries. Sex differentiation of the hypothalamus is not, therefore, involved in the selective surge of FSH. J. Endocr. (1985) 106, 31–36


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