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PubMed1988

Pulsatile GnRH treatment of the ovariectomized rat and release of LH and FSH.

The effect of pulsatile GnRH administration on the levels of LH and FSH was investigated in rats that had been ovariectomized 2 weeks earlier. Also the asynchronous occurrence of endogenous and GnRH-induced LH and FSH pulses was analysed. A small pulse dose of GnRH (1.25 ng/100 g) was given iv at a frequency of once every 60 min or once every 120 min during 24 h. A larger dose of 5 ng/100 g was given once every 60 or 120 min during either 24 h or 96 h. Blood was sampled arterially every 5 min around the two first and last GnRH injections and LH and FSH were measured. Only the treatment with the larger GnRH pulse dose resulted in a change of LH and FSH plasma levels. LH levels declined under all circumstances, whereas FSH was found to be increased temporarily after 24 h of treatment. The pituitary LH response to pulses of GnRH (5 ng/100 g) decreased irrespective of the frequency or duration with which GnRH was administered. There was a marked asynchronicity between LH and FSH pulses and almost every injection of GnRH (5 ng/100 g) resulted in clear LH pulses but not in FSH pulses.

Animals↗
PubMed1990

Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: hormonal and immunocytochemical studies.

The case of a 7-year-old boy affected with precocious puberty and a large intra- and suprasellar pituitary tumour is described. He had hyperprolactinemia and elevated serum LH, FSH and testosterone concentrations. Pre-operative dynamic hormonal studies showed a rise of PRL, LH and FSH levels after TRH (200 micrograms iv) and a rise of LH and FSH after GnRH (100 micrograms iv). Dopamine infusion (4 micrograms.kg-1.min-1 for 180 min) did not affect gonadotropins and greatly reduced serum PRL. GnRH analogue (buserelin, 0.5 mg sc t.i.d. for 10 days) administration inhibited both LH and FSH, but did not affect PRL concentration. Serum LH and FSH increased after ethinyl-estradiol (0.5 mg orally) administration, and were not affected by bromocriptine (5-7.5 mg/day for 10 days), which decreased serum PRL levels. The patient underwent transfrontal neurosurgery and a large tumour mass was completely removed. Morphological study of the excised tumour, by electron microscope double label immunotechnique, revealed that a large number of tumour cells (70-85%) were positive for PRL, LH and FSH, co-localized in the same secretory granule. After neurosurgery, serum PRL, LH, FSH and testosterone levels fell to within the normal limits. Two months later the patient was well and signs of precocious puberty had partially regressed; hormone levels were in the normal range and MR imaging control did not demonstrate any residual lesion in the sellar region.

Adenoma↗
PubMed1996

Long-term GnRH-agonist administration revealed a GnRH-independent mechanism stimulating FSH discharge in humans.

The present study evaluated the FSH and LH episodic discharge in different physiopathological conditions undergoing chronic GnRH-agonist administration. Four girls with true precocious puberty and five postmenopausal women were administered GnRH-agonist (3.73 leuprolide acetate every 4 weeks; Takeda Italia, Rome, Italy) for at least 4 months. Plasma LH and FSH secretory profiles were assessed before and under GnRH-agonist administration (after 21 and 120 days). Pulsatility studies were conducted for 4 h in the girls and for 6 h in postmenopausal women, with blood sampling intervals of 10 min. Pubertal and postmenopausal patients showed the distinct episodic co-secretion of LH and FSH before GnRH-agonist administration; this co-secretion disappeared in both groups after 21 and 120 days of treatment. Moreover, while LH concentrations decreased to almost undetectable levels and LH episodic release disappeared, FSH plasma levels were only partially reduced and FSH episodic secretion was detectable in both groups. In conclusion, this study demonstrated that long-term GnRH-agonist administration blocked LH but not FSH episodic release. These data enforce the hypothesis that FSH episodic discharge might be dependent not only on hypothalamic GnRH, but also on a GnRH-independent stimulatory pathway.

Child↗
PubMed2000

Signaling between the pituitary gland and the testes: inverse relationship between serum FSH and inhibin B concentrations in boys in early puberty.

OBJECTIVES: To study the relationship between serum inhibin B and sex steroid concentrations and pituitary FSH responsiveness to GnRH in boys in early puberty, and to examine serum inhibin B levels in prepubertal boys with different timing of the onset of gonadotropin deficiency (GD). DESIGN: Twenty-five boys with constitutional delay of puberty (CDP; 20 in Tanner stage G2 and 5 in G3; age range, 13. 5-16.8 years) and eight prepubertal boys (G1P1) with GD (age range, 10.0-13.2 years) were clinically examined, and serum inhibin B, testosterone and estradiol concentrations were measured from sera obtained immediately before the administration of GnRH (Relefact; 3.5 microgram/kg, maximum 100 microgram i.v.). Thereafter, FSH levels were measured at 30min intervals up to 90min. RESULTS: In the boys with CDP, basal inhibin B and FSH levels did not correlate. However, inhibin B and GnRH-stimulated FSH concentrations (r(S)= -0.43 to -0.45, n=25, P<0.05) and the difference between basal and peak serum FSH levels were inversely related (r(S)= -0.63, n=25, P<0.005). This relationship remained significant in boys at stage G2 (r(S)= -0.66, n=20, P<0.005). Basal testosterone concentrations and GnRH-induced FSH levels did not correlate. Estradiol levels were too low (64% of the boys had estradiol levels below the assay sensitivity) to allow correlation analysis. The boys with GD had low inhibin B concentrations (range, <15.6-53pg/ml); the lowest levels were observed in boys with presumably congenital onset of the disease. Serum inhibin B levels and testis volumes correlated positively (r(S)=0.70, n=8, P=0.07). CONCLUSIONS: These results suggest that, in boys, the reciprocal regulation between inhibin B and FSH is in operation before mid-puberty. Moreover, autonomous inhibin B secretion by the prepubertal human testis is likely to reflect the number of Sertoli cells.

Adolescent↗
PubMed2002

Serum inhibin B, FSH, LH and testosterone levels before and after human chorionic gonadotropin stimulation in prepubertal boys with cryptorchidism.

BACKGROUND: Several studies have indicated that cryptorchidism is associated with degenerative changes in both Sertoli cells and germ cells. The gonadal peptide hormone inhibin B reflects Sertoli cell function. Low inhibin B levels are found in a large portion of formerly cryptorchid men who show compromised seminiferous tubule function. It is not known if inhibin B can be used to demonstrate early damage of seminiferous tubules in prepubertal boys with cryptorchidism. METHODS: We investigated the relationship between serum levels of inhibin B, testosterone, FSH and LH in 62 prepubertal boys with uni- and bilateral cryptorchidism. Furthermore, we investigated the changes in serum levels of inhibin B and the corresponding changes in serum levels of FSH, LH and testosterone during a short course (3 weeks) of human chorionic gonadotropin (hCG) injections in 18 of these cryptorchid boys. RESULTS: In the 62 prepubertal boys with uni- or bilateral cryptorchidism there were no significant differences in baseline levels (median and range) of inhibin B (88 (20-195) pg/ml vs 78 (35-182) pg/ml; not significant), LH (0.08 (<0.05-0.99) IU/l vs 0.06 (<0.05-1.61) IU/l; not significant) and FSH (0.60 (0.08-3.73) IU/l vs 0.85 (0.25-2.55); not significant) compared with 156 healthy prepubertal boys, and there were no differences in hormonal levels between boys with uni- or bilateral cryptorchidism. There was no correlation between baseline levels of inhibin B and FSH. In boys younger than 9 years, we found no correlation between baseline levels of inhibin B and LH whereas, in boys older than 9 years, baseline levels of inhibin B were positively correlated to baseline LH (Spearman rank correlation coefficient ((R(s))=0.58, P=0.03). Treatment with hCG (1500 IU intramuscularly twice weekly for 3 weeks) resulted in descensus of testes in 9 out of 18 patients. In all boys but one, irrespective of age, hCG induced a marked increase in testosterone into the adult range (from undetectable to 21.8 (7.0-35.4) nmol/l; P<0.001) and completely suppressed FSH and LH levels. Serum levels of inhibin B increased significantly from 116 (50-195) pg/ml to 147 (94-248) pg/ml (P<0.05), but not uniformly. The increase in serum levels of inhibin B was inversely correlated to baseline inhibin B (Rs=-0.52, P=0.03) and baseline FSH (R(s)=-0.59, P<0.01). CONCLUSIONS: We therefore suggest that, in the prepubertal testes, inhibin B is secreted from the prepubertal Sertoli cells following hCG, whereas early pubertal testes with more differentiated Sertoli cells are not able to secrete inhibin B in response to hCG stimulation, perhaps due to lack of germ cell-derived betaB-subunits. We found (a) normal inhibin B levels in prepubertal boys with uni- or bilateral cryptorchidism, (b) that hCG stimulated testosterone markedly and suppressed FSH and LH levels and (c) that hCG treatment stimulated inhibin B levels in the youngest cryptorchid boys. In the oldest prepubertal boys no hCG-induced changes in inhibin B were shown.

Adolescent↗
PubMed2005

Does metformin modify ovarian responsiveness during exogenous FSH ovulation induction in normogonadotrophic anovulation? A placebo-controlled double-blind assessment.

OBJECTIVE: To assess whether the addition of metformin to gonadotrophin ovulation induction in insulin-resistant, normogonadotrophic, anovulatory women alters ovarian responsiveness to exogenous FSH. DESIGN: Placebo-controlled double-blind assessment in an academic hospital. RESULTS: After a progestagen withdrawal bleeding, patients were randomised for either metformin (n = 11) or placebo (n = 9) treatment. In cases of absent ovulation, exogenous FSH was subsequently administered to induce ovulation. Only during metformin treatment did body mass index and androgen (androstenedione and testosterone) levels decrease, whereas FSH and LH levels increased significantly. In the metformin group, a single patient ovulated before the initiation of exogenous FSH. Significantly more monofollicular cycles and lower preovulatory oestradiol concentrations were observed in women receiving FSH with metformin compared with FSH alone. CONCLUSIONS: Metformin co-treatment in a group of insulin-resistant, normogonadotrophic, anovulatory patients resulted in normalization of the endocrine profile and facilitated monofollicular development during the FSH induction of ovulation.

Adolescent↗
PubMed1975

Variations in serum FSH, LH and testosterone levels in male rats from birth to sexual maturity.

Serum LH, FSH and testosterone concentrations were measured by radioimmunoassays in male Sprague-Dawley rats from birth to 80 days of age. The levels of FSH were significantly elevated during the first 5 days of postnatal life. An abrupt decline in FSH concentrations occurred during this period, from levels of 800 ng/ml on day 1 to levels of 300 ng/ml on Day 6. Subsequently, FSH levels fluctuated widely until about Days 30 to 45, when a secondary peak of FSH was observed. Thereafter, a decline in FSH levels to those found in adult rats occurred. This decline in FSH levels appears to coincide with the first release of mature spermatozoa from the germinal epithelium in the testis. During the first 30 days of postnatal life, LH and testosterone values appeared to be inversely related to each other and an LH peak and a nadir of testosterone levels was observed between Days 6 and 14 at time corresponding to regression of the fetal generation of interstitial cells. A parallel rise in LH and testosterone levels occurred from Days 30 to sexual maturity and corresponded to the development of the adult generation of intestitial cells.

Age Factors↗
PubMed1980

Possible involvement of inhibin in the interrelationship between numbers of antral follicles and peripheral FSH concentrations in female rats.

The possible dependence of peripheral concentrations of FSH on a non-steroidal, ovarian factor, was studied in adult female rats. Increases in FSH levels during the periovulatory period were not correlated with decreases of steroid concentrations, and administration of steroids did not result in a reduction of FSH levels to basal values. However, a negative correlation between FSH levels and numbers of large follicles (volume greater than or equal to 200 x 10(5) micron 3) was demonstrated, and injection of steroid-free bovine follicular fluid, which contains inhibin-like activity, suppressed FSH levels to basal values. These results suggest that an ovarian, inhibin-like factor is involved in the fast regulation of FSH concentrations in the periovulatory period, and that this inhibin-mediated control of FSH might play a role in the regulation of the number of follicles maturing in female rats.

Animals↗
PubMed1984

Modulatory action of FSH on LH-induced follicular growth in rats.

Three to four ovaries from rats on the day of di-oestrus I were placed in perifusion culture at 10:30 h and exposed to (1) no gonadotrophin (in-vitro controls); (2) tonic FSH (200 ng RP-1/ml); (3) tonic LH (30 ng RP-1/ml); (4) tonic FSH + tonic LH; or (5) tonic FSH plus hourly pulses of LH (amplitude = 50 ng/ml). The total amount of LH administered was 3060 ng RP-1 regardless of mode of delivery. After culture for 3 h, the ovaries were prepared for histological analysis. Compared to in-vitro controls, tonic LH stimulation increased the number of follicles with greater than 1.6 X 10(5) granulosa cells (P less than 0.05); it was estimated that each follicle in the larger size class increased by 5.5 +/- 2.7 X 10(4) cells. Tonic FSH or tonic FSH + tonic LH treatment did not promote growth into the 1.6 X 10(5) cell class. In the presence of tonic FSH, hourly LH pulses induced follicular growth similar to that observed after tonic LH treatment. The data demonstrate that LH promotes the growth of follicles in vitro. FSH modulates this stimulatory action of LH, allowing it to be expressed when LH is administered in hourly pulses.

Animals↗
PubMed1986

Effects of FSH and LH on incorporation of [3H]thymidine into follicular DNA.

To assess the roles of FSH and LH on follicular growth, after various experimental manipulations, hamster follicles were sorted into 10 stages and incubated for 4 h with [3H]thymidine. Stages 1-4 correspond to follicles with 1-4 layers of granulosa cells, respectively; Stage 5 = 5 or 6 layers of granulosa cells plus theca; Stage 6 = 7-8 layers of granulosa cells plus theca; Stage 7 = early formation of the antrum; Stages 8-10 = small, intermediate and large antral follicles, respectively. Phenobarbitone sodium injected at 13:00 h on pro-oestrus blocked the normal rise of blood FSH and LH concentrations at 15:00 h and prevented the increase of [3H]thymidine incorporation into follicles of Stages 1-9. The optimal treatment to reverse the effects of phenobarbitone was 1 microgram FSH and 2 micrograms LH injected i.p. at 13:00 h which restored DNA replication to follicles of Stages 2-10: FSH acted primarily on Stages 2-5 and LH on Stages 5-10. Injection of phenobarbitone at 13:00 h on prooestrus followed by 2.5 micrograms FSH at 22:00 h restored DNA synthesis by the next morning to follicles at Stages 1-8. In hamsters hypophysectomized at 09:00 h on the day of oestrus (Day 1), injection on Day 4 of 2.5 micrograms FSH restored DNA synthesis 6 h later to Stage 2-6 follicles. Unilateral ovariectomy on Day 3 resulted 6 h later in an acute rise in FSH and LH and change of follicles from Stage 4 to Stage 5 but, paradoxically, there was decreased synthesis of DNA in follicles of Stages 5-10.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Role of the peripubertal pattern of FSH, LH and prolactin secretion in regulating in-vitro steroidogenesis and follicular growth within juvenile rat ovaries.

Juvenile rat ovaries were placed in perifusion culture and exposed to (1) tonic FSH (200 ng PR-1 equiv./ml), (2) LH pulses (2/h, amplitude = 80 ng RP-1 equiv./ml), (3) tonic FSH and LH pulses, (4) tonic FSH with LH mini-surges, or (5) tonic FSH with LH and prolactin mini-surges. The LH mini-surge consisted of a series of 80 ng/ml pulses (2/h) with LH increasing to 180 ng/ml for 2 h then returning to the 80 ng/ml pulses. The prolactin mini-surge consisted of a series of 15 ng/ml pulses (2/h) with prolactin increasing to 40 ng/ml for 2 h before returning to the 15 ng/ml pulses. The LH mini-surge occurred at 14:00 h daily while a prolactin mini-surge occurred at 14:00 h and 06:00 h daily. Ovaries were perifused for 0 (in-vivo control), 24 or 48 h, incubated for 1 h in hormone-free medium to assess steroid secretion and subsequently prepared for histological analysis. After a 24 h exposure to FSH, oestradiol secretion was increased, while exposure to LH pulses enhanced progesterone secretion. Treatment with FSH, LH pulses or FSH plus LH pulses decreased the number of small antral follicles by 24 h of perifusion compared to control (P less than 0.05). The LH mini-surge maintained the small and medium-sized antral follicles after 24 h and increased the number of preovulatory-sized follicles over controls by 48 h (P less than 0.05). Prolactin/LH mini-surges increased the number of preovulatory-sized follicles within 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

GnRH-dependent and -independent components of FSH secretion after acute treatment of anoestrous ewes with ovine follicular fluid and a GnRH antagonist.

Gonadotrophin and inhibin concentrations were measured in anoestrous ewes after acute treatment with either saline, ovine follicular fluid (oFF), GnRH antagonist, or oFF and GnRH antagonist in combination. The increase in mean LH concentrations observed in ewes treated with oFF alone, was not seen in either of the groups treated with GnRH antagonist, in which LH pulsatility was completely inhibited. This result suggests that the LH rebound that follows follicular fluid treatment is GnRH dependent. Blockade of GnRH had no effect on the suppression of FSH seen after follicular fluid injection, indicating that this component of FSH secretion is independent of short-term GnRH input. After this initial suppression, a rebound release of FSH was seen in the group treated with oFF alone. The addition of GnRH antagonist appeared to decrease the rebound, suggesting that this rebound release of FSH may have a GnRH-dependent component. Inhibin concentrations in both oFF-treated groups increased after oFF injection and then declined to pretreatment values. However, a second rise in inhibin concentration, concomitant with the FSH rebound in ewes receiving oFF alone, was seen in the group treated with oFF and GnRH antagonist. As this rise in endogenous inhibin concentration could also act to suppress the rebound release of FSH, it cannot be conclusively proved from this study that GnRH input is required for the generation of the rebound release of FSH after treatment with oFF.

Anestrus↗
PubMed1997

Effect of immunization of rams against bovine inhibin alpha 1-26 on semen characteristics, scrotal size, FSH, LH and testosterone concentrations.

The effects of inhibin immunization on inhibin antibody titres, semen characteristics, scrotal size, fertility, FSH, LH and testosterone concentrations were determined by immunizing adult rams against bovine inhibin alpha 1-26-Gly-Tyr conjugated to human serum albumin (n = 16) in non-ulcerative Freund's adjuvant and DEAE:dextran (1:1) or adjuvant alone (n = 16) on days 0 (29 June), 30, 60, 191, 303 and 394. Blood samples were collected and bovine inhibin alpha 1-26-Gly-Tyr antibody titres and serum testosterone concentrations were determined. Each month, between days 174 and 417, semen was collected every 30 min to a maximum of 15 ejaculates over 7 h and scrotal circumference was measured. Ram fertility was recorded during natural service. FSH, LH and testosterone concentrations and GnRH-induced FSH and LH release were measured in a subgroup of immunized (n = 5) and control (n = 5) rams at frequent intervals. Antibody titres were variable among immunized rams (0-46% 125I-labelled bovine inhibin alpha 1-26-Gly-Tyr at 1:1600 serum dilution) but mean titres were consistently higher than in control rams (P < or = 0.001). Immunization did not alter the semen volume, output or quality of spermatozoa or ram fertility, but increased the mean scrotal circumference (37.6 +/- 0.8 cm versus 34.4 +/- 0.7 cm, P < 0.001). Mean FSH concentrations were higher in immunized rams during two intensive blood sampling periods (in June and August) (5.8 +/- 0.7 ng ml-1 versus 3.0 +/- 0.3 ng ml-1, P < 0.001 in June; and 4.8 +/- 0.9 ng ml-1 versus 2.0 +/- 0.3 ng ml-1, P < 0.02 in August), and were correlated with antibody titres (r2 = 0.3, P < 0.05 in June; and r2 = 0.8, P < 0.001 in August). Discrete FSH pulses were not detected. Immunization did not alter mean or basal testosterone or LH concentrations, or LH pulse frequency; LH pulse amplitude was increased (1.6 +/- 0.2 ng ml-1 versus 0.8 +/- 0.2 ng ml-1, P < 0.02) and was correlated with antibody titres (r2 = 0.6, P < 0.01). Immunization enhanced GnRH-induced FSH (P < 0.05) but not LH release. In conclusion, immunization of adult rams against bovine inhibin alpha 1-26 Gly-Tyr increased scrotal circumference, mean FSH concentrations and LH pulse amplitude, without altering semen characteristics, fertility, mean LH concentrations, LH pulse frequency or mean testosterone concentrations.

Animals↗
PubMed2001

Is there an FSH-releasing factor?

A thorough understanding of the factors that regulate the secretion of FSH is critical for the development of efficient methods for fertility regulation. The purpose of this review is to evaluate what is currently known about the existence of FSH-releasing factor(s). It considers the obstacles encountered in understanding the control of FSH secretion, current knowledge of the nature of FSH secretion and the mechanisms involved in controlling FSH secretion, the arguments that have been posed against the need for an FSH-releasing factor and finally the evidence available to date supporting the existence of FSH-releasing factor(s).

Animals↗
PubMed2004

Evidence that lamprey GnRH-III does not release FSH selectively in cattle.

Experiments were performed to test the hypothesis that lamprey GnRH-III (lGnRH-III) selectively releases FSH. Primary cultures of bovine adenohypophyseal cells were treated with mammalian GnRH (mGnRH) and lGnRH-III (10(-9), 10(-8), 10(-7) and 10(-6) M) or control media in Experiment 1. All doses of mGnRH and the two highest doses of lGnRH-III stimulated (P < 0.001) a non-selective release of LH and FSH. In Experiments 2-4, Latin Square designs were utilized in vivo to examine whether physiological and hormonal milieu regulate putative selective effects of lGnRH-III. In Experiments 2 and 3, ovariectomized cows with basal levels of estradiol only (Experiment 2) or in combination with luteal phase levels of progester-one (Experiment 3) were injected with mGnRH and lGnRH-III (0.055, 0.11, 0.165 and 1.1 microg/kg body weight (BW) and saline. All doses of mGnRH released (P < 0.001) LH and FSH, but only the highest dose of lGnRH-III stimulated (P < 0.001) a non-selective release of both LH and FSH (Experiment 3). For Experiments 4A and 4B, intact, mid-luteal phase cows were injected with mGnRH and lGnRH-III (1.1 microg/kg BW; Experiment 4A), lGnRH-III (1.1 and 4.4 microg/kg BW; Experiment 4B) and saline. As before, mGnRH released (P < 0.001) both LH and FSH at all doses. In contrast, lGnRH-III at the highest dose released (P < 0.001) LH but not FSH. These findings suggest that lGnRH-III may act as a weak competitor for the mGnRH receptor and do not support the hypothesis that it selectively releases FSH in cattle.

Animals↗
PubMed1975

Response of serum LH, FSH and prolactin to injection of synthetic LH-RH into rat anterior pituitary.

Changes in serum LH, FSH and prolactin were measured by radioimmunoassay following injection of synthetic LH-RH into the anterior pituitary and median eminence of rats. The time course of serum levels of LH and FSH after injection of synthetic LH-RH into the pituitary showed a peak at 15 min. The synthetic LH-RH had a more marked releasing effect on LH than on FSH. After injection of 20 ng into the pituitary, the serum LH rose to about 10.7 times the control level but the serum FSH only to about 1.8 times. A significant rise of serum LH over the control level was noted after injection of more than 0.2 ng of synthetic LH-RH, while that of serum FSH was after injection of more than 2 ng. An injection of 2 ng of synthetic LH-RH into the pituitary following 0.1 mug of estradiol benzoate resulted in a fall of serum LH and FSH levels, and a rise of serum prolactin level. An injection of 2 ng of synthetic LH-RH into the median eminence resulted in a tendency towards slight decrease in serum LH and FSH. No significant response of serum prolactin to synthetic LH-RH was noted.

Animals↗
PubMed1976

Dynamic changes of serum LH and FSH during pregnancy and puerperium.

Changes of serum LH (HCG) and FSH, and their response to LH-RH during pregnancy and puerperium were studied by radioimmunoassay. There was little change in serum FSH level due to progression of pregnancy, and the serum FSH level of pregnant women was almost unchanged after injection of LH-RH. Serum LH (HCG) which decreased rapidly after delivery returned at about 15 days after parturition, and FSH which remained at a low level during pregnancy returned to the levels in the follicular phase of the normal women at about 20 days after delivery. The alteration in the response to LH-RH in puerperal period was as follows: First FSH began to respond about 10 days after delivery, and one month after parturition both LH and FSH showed remarkable response in comparison with that in the normal non-pregnant period. Beyond the second postpartal month, the response of FSH returned to approximately the same level as that in the normal non-pregnant period, but the response of LH was still marked when compared with that in the non-pregnant period. There were no differences in the response to LH-RH between the nursing and non-nursing women.

Breast Feeding↗
PubMed1987

Blockade of the final phase of ovulation has no effect on the post-ovulatory surge of serum FSH in the rabbit.

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.

Animals↗