Induction of the gonadotrophin surge-inhibiting factor by FSH and its elimination: a sex difference in the efficacy of the priming effect of gonadotrophin-releasing hormone on the rat pituitary gland

1993 ◽  
Vol 138 (2) ◽  
pp. 191-201
Author(s):  
D. W. Koppenaal ◽  
J. A. M. J. van Dieten ◽  
A. M. I. Tijssen ◽  
J. de Koning
Keyword(s):  
Body Weight ◽  
Pituitary Gland ◽  
Priming Effect ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Pulse Interval ◽  
Intact Female ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone

ABSTRACT This study was designed to explore the efficacy of gonadotrophin-releasing hormone (GnRH) to antagonize the effect of gonadotrophin surgeinhibiting factor (GnSIF) on the timing of the induction by GnRH of the maximal self-priming effect on pituitary LH responsiveness. The GnSIF levels were increased by FSH treatment and reduced after gonadectomy. Female rats were injected s.c. with 10 IU FSH or saline (control) on three occasions during the 4-day cycle. Serial i.v. injections of GnRH (500 pmol/kg body weight) were administered to intact rats on the afternoon of pro-oestrus or 15–30 min after ovariectomy. Intact male rats were given 10 IU FSH and 500 or 2000 pmol GnRH/kg body weight on an equivalent time-schedule. Endogenous GnRH release was suppressed with phenobarbital. In intact female control rats, the timing of the maximally primed LH response was delayed as the GnRH pulse-interval increased. FSH treatment of female rats induced a suppression of the initial unprimed LH response and delayed the maximally primed LH response, which showed further delay as the GnRH pulse-interval was increased. When the pulsatile administration of GnRH was started 15–30 min after ovariectomy, the priming effect of GnRH did not change as the GnRH pulse-interval was increased in the saline-treated rats. However, FSH treatment caused a suppression of the unprimed LH response, a delay in the primed LH response and decreased the delay of the maximally primed LH response to GnRH when the GnRH pulse-interval was decreased. Increasing the interval between ovariectomy and the first GnRH pulse to 4 h diminished the efficacy of the FSH treatment: GnRH-induced priming was delayed by only one pulse instead of the two pulses in control rats. In intact males but not in orchidectomized rats, a self-priming effect was demonstrated during GnRH pulses which were 1 h apart. The effect of 2 nmol GnRH/kg body weight was the most pronounced. Compared with intact female rats, the timing of the maximally primed LH response was delayed by 1 h. FSH treatment did not affect the pituitary LH response to both dose levels of GnRH. It is concluded that FSH treatment increased the release of GnSIF by the ovary, then induced a state of low responsiveness of the pituitary gland to GnRH and subsequently delayed GnRH-induced maximal self-priming. The efficacy of GnRH to prime the pituitary gland was higher when GnSIF levels were decreasing after removal of the ovaries. On the other hand, GnSIF was more effective when the GnRH pulse-interval was increasing. This allows GnSIF more time to restore the unprimed state of the pituitary gland after each GnRH pulse-induced self-priming effect. It remains a matter of debate whether a similar mechanism of action is present in the male rat or whether this mechanism is suppressed by endogenous hormones such as androgens. Journal of Endocrinology (1993) 138, 191–201

IN-VITRO STUDIES OF THE EFFECTS OF OESTROGEN PRETREATMENT ON THE SENSITIVITY OF THE IMMATURE FEMALE RAT PITUITARY GLAND TO STIMULATION WITH GONADOTROPHIN RELEASING HORMONE

1977 ◽  
Vol 74 (1) ◽  
pp. 11-21 ◽  
Author(s):  
M. WILKINSON ◽  
D. DE ZIEGLER ◽  
DANIELLE CASSARD ◽  
K. B. RUF
Keyword(s):  
Pituitary Gland ◽  
Brain Lesion ◽  
Culture Technique ◽  
Female Rats ◽  
Female Rat ◽  
Immature Female ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Unilateral Brain Lesion

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.

THE EFFECTS OF TESTOSTERONE AND ITS 5α-REDUCED METABOLITES ON PITUITARY RESPONSIVENESS TO GONADOTROPHIN-RELEASING HORMONE (Gn-RH)

1977 ◽  
Vol 86 (4) ◽  
pp. 728-732 ◽  
Author(s):  
Y. Epstein ◽  
B. Lunenfeld ◽  
Z. Kraiem
Keyword(s):  
Pituitary Gland ◽  
Mature Male ◽  
Male Rats ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Low Levels ◽  
High Doses ◽  
Dose Dependent ◽  
Stimulation Of

ABSTRACT The aim of this study was to investigate effects of androgens on gonadotrophin release in response to gonadotrophin-releasing hormone (Gn-RH) stimulation in vitro. Hemipituitaries of mature male rats were pre-incubated for 90 min with T, DHT, 3α- or 3β-diol (4 ng or 4 μg/ml medium), and the incubation continued for 240 min after adding Gn-RH (1 ng/ml medium). Gn-RH caused a 4-5-fold rise in the secretion of LH and a 2-fold rise in FSH secretion. The effect of the androgens was dose-dependent. At low levels, T and DHT exerted no effect on Gn-RH-stimulated gonadotrophin release, whereas the two androstanediols (3α- and 3β-diol) augmented the Gn-RH stimulation of both gonadotrophins, though preferentially LH. With high doses of androgens, the results obtained showed: a) no effect of T; b) DHT suppression of the Gn-RH-stimulated FSH release; c) suppression of Gn-RH stimulation by 3α- and 3β-diol regarding both LH and FSH. It is concluded that T exerts through its reduced metabolites a feedback effect on the pituitary gland responsiveness to Gn-RH stimulation.

Hyperprolactinaemia attenuates the gonadotrophin releasing hormone receptor response to gonadectomy in rats

1982 ◽  
Vol 95 (2) ◽  
pp. 267-274 ◽  
Author(s):  
R. N. Clayton ◽  
L. C. Bailey
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Serum Prolactin ◽  
Intact Male ◽  
Adult Rats ◽  
Releasing Hormone ◽  
Receptor Response ◽  
Serum Lh ◽  
Gonadotrophin Releasing Hormone ◽  
Qualitative Index

Measurement of pituitary gonadotrophin releasing hormone (Gn-RH) receptor content provides a qualitative index of prior exposure of the pituitary gland to endogenous Gn-RH. The effect of moderate hyperprolactinaemia (serum prolactin = 95–250 μg/l), achieved with three pituitary grafts beneath the renal capsule, on the pituitary Gn-RH receptor content and serum LH responses to gonadectomy of adult rats has been studied. In males the presence of hyperprolactinaemia for 7 days completely prevented the increase in Gn-RH receptor content 3 days after castration and inhibited the serum LH rise by 45%. By 6 days after castration, Gn-RH receptors had increased in the hyperprolactinaemic castrated animals but values were 33% lower than in sham-grafted controls, while the serum LH increase was attenuated by 30%. Pituitary LH content was also lower in grafted castrated animals 6 days after castration. Hyperprolactinaemia for 3 weeks had no effect on Gn-RH receptors or pituitary LH content of intact male rats, although basal serum LH was decreased by 50%. Hyperprolactinaemia also attenuated the increases in Gn-RH receptors, serum LH and pituitary LH which occurred 6 days after ovariectomy in female rats. In all experiments the pituitary content of prolactin was reduced by 80–90% in animals bearing pituitary grafts. These results suggest that hyperprolactinaemia restricts the Gn-RH receptor response to gonadectomy by decreasing endogenous hypothalamic Gn-RH secretion.

Anaesthesia with alphaxalone plus alphadolone acetate decreases serum concentrations of LH in castrated rats

1987 ◽  
Vol 115 (2) ◽  
pp. 221-223 ◽  
Author(s):  
M. A. Emanuele ◽  
J. Tentler ◽  
L. Kirsteins ◽  
D. Reda ◽  
N. V. Emanuele ◽  
...  
Keyword(s):  
Time Dependent ◽  
Female Rats ◽  
Male Rat ◽  
Serum Concentrations ◽  
Releasing Hormone ◽  
Reproductive Unit ◽  
Gonadotrophin Releasing Hormone ◽  
Neuroendocrine Axis

ABSTRACT Alphaxalone is considered the anaesthetic of choice in neuroendocrine reproductive studies in female rats, since it appears to have little, if any, effect on release of gonadotrophin-releasing hormone. There has been less study of the effects of this anaesthetic on the male reproductive neuroendocrine axis, however. Accordingly, the time-dependent effects of alphaxalone, as well as of urethane and ketamine, on the increased levels of LH in castrated rats were determined. Each anaesthetic was administered i.p. and each depressed LH levels significantly compared with those in castrated unanaesthetized rats killed by decapitation (controls). The effect of the anaesthetics was noted 15 min after administration and persisted at 30 and 60 min in animals anaesthetized with alphaxalone and urethane. Only in ketamine-anaesthetized animals did serum concentrations of LH finally rise to concentrations not significantly different from those in control rats. Thus alphaxalone, though useful in female neuroendocrine studies, is as profoundly disruptive as other anaesthetics on the male rat hypothalamic-pituitary reproductive unit. J. Endocr. (1987) 115, 221–223

EFFECT OF ACTIVE IMMUNIZATION TO LUTEINIZING HORMONE RELEASING HORMONE ON SERUM AND PITUITARY GONADOTROPHINS, TESTES AND ACCESSORY SEX ORGANS IN THE MALE RAT

1974 ◽  
Vol 63 (2) ◽  
pp. 399-NP ◽  
Author(s):  
H. M. FRASER ◽  
A. GUNN ◽  
S. L. JEFFCOATE ◽  
DIANE T. HOLLAND
Keyword(s):  
Luteinizing Hormone ◽  
Active Immunization ◽  
Male Rats ◽  
Male Rat ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Accessory Sex Organs ◽  
Gonadotrophin Releasing Hormone ◽  
Low Levels ◽  
Lh Rh

SUMMARY Autoimmunity to luteinizing hormone releasing hormone (LH-RH) in adult male rats, induced by immunization with LH-RH conjugated to bovine serum albumin, resulted in atrophy of the testes and secondary sex organs and aspermatogenesis. Both immunoreactive luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in serum and the pituitary were reduced to low levels compared with those of control animals. It is suggested that antibodies to LH-RH can inhibit the action of endogenous hormone and that LH-RH is, in fact, the gonadotrophin-releasing hormone in the rat, required for the release of both LH and FSH.

Gonadotrophin-releasing hormone regulation of gonadotrophin subunit gene expression: studies in tri-iodothyronine-suppressed rats

1989 ◽  
Vol 122 (1) ◽  
pp. 117-125 ◽  
Author(s):  
D. J. Haisenleder ◽  
G. A. Ortolano ◽  
A. C. Dalkin ◽  
S. J. Paul ◽  
W. W. Chin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Blot Hybridization ◽  
Male Rats ◽  
Male Rat ◽  
Mrna Levels ◽  
Dot Blot ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Prolactin Mrna

ABSTRACT We have previously shown that a pulsatile gonadotrophin-releasing hormone (GnRH) stimulus can increase steady-state levels of α and LH-β subunit mRNAs in the male rat pituitary. Since α subunit is produced in both thyrotroph and gonadotroph cells, the effect of GnRH specifically on gonadotroph α gene expression is uncertain. To address this tissue, adult male rats were given injections of tri-iodothyronine (T3; 20 μg/100 g body wt, i.p.) daily for 8 days (day 8 = day of death) in order to decrease thyrotroph α mRNA levels (+ T3 group). Saline injections (i.p.) were given to control animals (− T3 group). Three days before GnRH administration, the animals were castrated and testosterone implants inserted s.c., to inhibit endogenous GnRH secretion. GnRH pulses (25 ng/pulse; 30-min interval) were given to freely moving animals (saline pulses to controls) via an atrial cannula for 12, 24 or 48 h. Serum LH and FSH were measured before and 20 min after the last GnRH pulse. Pituitary RNA was extracted and α, LH-β, FSH-β and prolactin mRNA levels were determined by dot-blot hybridization using 32P-labelled cDNA probes. Castration and testosterone replacement reduced α and LH-β mRNA levels by 30 and 40% respectively, compared with levels in untreated intact males, but did not decrease FSH-β concentrations. T3 administration further decreased α mRNA to 30% of values seen in intact males, but LH-β mRNA levels were unchanged. FSH-β mRNA concentrations were decreased by 23% in T3-treated rats (P < 0·05 vs intact controls). In −T3 rats, 12 h of GnRH pulses increased FSH-β mRNA levels (twofold) vs saline-pulsed controls, but significant increases in α or LH-β mRNA levels were not seen until after 24 h of GnRH pulses. In the +T3 group, an increase in α mRNA was observed earlier, after 12 h of GnRH pulses. After 24 and 48 h of GnRH, the increments in α and LH-β were of similar magnitude in both the +T3 and − T3 groups (4–5 and 3–4 fold increases in α and LH-β respectively; P < 0·05 vs saline-pulsed controls). In contrast, the stimulatory effect of GnRH on FSH-β mRNA was lost in + T3 animals after 48 h of pulses. In order to examine whether this loss in FSH-β mRNA responsiveness to GnRH was related to an inhibitory interaction of T3 in the presence of testosterone, a second study was conducted in castrated animals. The results showed that α mRNA levels were decreased by 33% in +T3 compared with −T3 castrated animals (P < 0·05), but LH-β and FSH-β mRNAs were unaffected by T3 administration. In castrated animals given GnRH pulses, T3 inhibited subunit mRNA responses and this effect was most marked for FSH-β mRNA. In contrast, prolactin mRNA levels were significantly higher (P < 0·05) in all +T3 experimental groups compared with their −T3 controls. These data indicate that T3 can inhibit FSH-β mRNA responses to pulsatile GnRH and that this action occurs in the absence of testosterone. Journal of Endocrinology (1989) 122, 117–125

EXPERIMENTAL STUDIES ON THE REGULATION OF CORPUS LUTEUM FUNCTION IN CASTRATED MALE RATS BEARING A TRANSPLANTED OVARY

1963 ◽  
Vol 43 (2) ◽  
pp. 246-254 ◽  
Author(s):  
G. H. Zeilmaker
Keyword(s):  
Pituitary Gland ◽  
Corpus Luteum ◽  
Functional Activity ◽  
Experimental Studies ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Corpora Lutea ◽  
Female Rat ◽  
Progesterone Production

ABSTRACT The functional activity of artificially induced corpora lutea in isologous ovaries transplanted into castrated male rats has been studied. Criteria for progesterone production were the morphology of vaginal transplants and the distribution of sudanophilic material in the corpus luteum cells. It was found that spontaneous functional activity of the corpora lutea did not occur in short-term experiments. Progesterone production was observed, however, in animals also bearing an isotransplanted (either male or female) pituitary gland, and in animals which received daily injections of reserpine. It is suggested that the normal influence of the central nervous system on the secretion of luteotrophic hormone is inhibitory in male as well as in female animals. Some aspects of the induction and maintenance of luteal function in castrated male rats bearing a transplanted ovary have been studied and compared with similar phenomena in the female rat. A real pseudopregnancy, i. e. maintained by the pituitary in situ during a defined period, as can be observed in female rats, could not be induced in these animals. In animals also bearing an isografted pituitary gland, luteolysis was not observed in experiments lasting up to 45 days. It is suggested that these findings may be correlated with the way in which the luteinizing hormone is secreted in the male rat.

Ontogeny of serum and pituitary gonadotrophins in male rats treated with low doses of 5α-dihydrotestosterone

1986 ◽  
Vol 108 (3) ◽  
pp. 369-375 ◽  
Author(s):  
S. Karanth ◽  
M. K. Gill ◽  
A. Dutt ◽  
N. Lehri ◽  
H. S. Juneja
Keyword(s):  
Body Weight ◽  
Male Rats ◽  
Male Rat ◽  
Low Doses ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Lh Releasing Hormone

ABSTRACT The effect of s.c. daily injections of 10 or 1000 ng 5α-dihydrotestosterone (DHT)/100 g body weight from birth to day 21, or from days 26 to 117 of age, on the changes in concentration of serum and pituitary gonadotrophins was investigated in male rats. Treatment with 10 ng DHT from days 1 to 21 depressed serum FSH, but not LH, at day 7, while 1000 ng DHT depressed both serum LH and FSH. Treatment with both doses of DHT reduced pituitary levels of LH and FSH at day 7, with FSH being more depressed than LH. Treatment with 10 ng DHT from days 26 to 117 increased serum FSH from days 82 to 117, while 1000 ng DHT did not have this effect. Treatment with 1000 ng, but not 10 ng, DHT between days 26 and 117 reduced pituitary levels of LH and FSH at day 40. Rats treated with the two doses of DHT from days 26 to 117 showed a difference in the responsiveness of the pituitary to LH-releasing hormone (LHRH). Treatment with 10 ng DHT enhanced LHRH-induced release of LH without affecting FSH release, while 1000 ng DHT depressed LHRH-induced release of FSH but not of LH. These findings support the view that DHT may play a modulatory role in the ontogeny of serum gonadotrophins and the responsiveness of the pituitary to LHRH during the onset of puberty in the male rat. J. Endocr. (1986) 108, 369–375

ONTOGENY OF THE SENSITIZING EFFECT OF OESTRADIOL AND LUTEINIZING HORMONE RELEASING HORMONE ON THE ANTERIOR PITUITARY GLAND OF THE FEMALE RAT

1981 ◽  
Vol 91 (2) ◽  
pp. 347-351 ◽  
Author(s):  
R. MEIDAN ◽  
G. FINK ◽  
Y. KOCH
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Priming Effect ◽  
Anterior Pituitary Gland ◽  
Female Rats ◽  
Facilitatory Effect ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

The ontogeny of the facilitatory effect of oestradiol and luteinizing hormone releasing hormone (LH-RH) on the responsiveness of the anterior pituitary gland to LH-RH has been studied in vitro using pituitary glands from female rats aged 15, 17, 20, 31, 35 and 38 days. The facilitatory effect of oestradiol was already well established by day 15, while the facilitatory effect of LH-RH (priming effect) developed only after day 17. Although it increased the overall response of the gland to LH-RH, oestradiol did not selectively enhance the priming effect of LH-RH. Both the effect of oestradiol and LH-RH reached a peak on day 25, 7 days before vaginal opening in this colony, and, as assessed by measuring pituitary LH contents, were not dependent upon the synthesis of LH. These data show that different mechanisms may be involved in the facilitation of pituitary responsiveness by oestradiol and LH-RH, but that both mechanisms appear to depend more upon an increase in the sensitivity of the receptor/release apparatus rather than in the gonadotrophin content of the gonadotrophs.

TESTICULAR RECEPTORS FOR LUTEINIZING HORMONE AFTER IMMUNONEUTRALIZATION OF GONADOTROPHIN RELEASING HORMONE IN THE MALE RAT

1977 ◽  
Vol 75 (1) ◽  
pp. 23-32 ◽  
Author(s):  
R. L. HAUGER ◽  
R. P. KELCH ◽  
YII-DER IDA CHEN ◽  
ANITA H. PAYNE
Keyword(s):  
Selective Reduction ◽  
Serum Testosterone ◽  
Pituitary Hormones ◽  
Male Rats ◽  
Male Rat ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Intact Male ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone

The effects of immunoneutralization of endogenous gonadotrophin releasing hormone (GnRH) on the serum concentrations of testosterone and gonadotrophins and the binding of 125I-labelled human chorionic gonadotrophin (HCG) to testicular membrane fractions were studied in adult male rats. Four days after the administration of 1 ml anti-GnRH serum, the level of testosterone in the serum decreased to 44% of the concentration before the injection, whereas administration of normal rabbit serum had no effect. Multiple injections of anti-GnRH serum for 4 days dramatically suppressed the secretion of gonadotrophins in rats orchidectomized 2 months earlier. In intact male rats treated identically, immunoneutralization of GnRH decreased the level of serum testosterone to 32% of the concentration present in saline-treated controls, but did not decrease the number of testicular binding sites for HCG (LH). Administration of testosterone or oestradiol for 3 or 6 days caused a marked reduction in the concentration of serum gonadotrophins but did not decrease the number of LH receptors. This study provides further support for the concept that one releasing hormone governs secretion of both FSH and LH. In addition, these studies indicate that selective reduction of gonadotrophins for 3–6 days has no effect on the number of testicular LH receptors. This suggests that pituitary hormones other than gonadotrophins may be important in the maintenance of testicular receptors for LH.

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