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.

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.

OESTRADIOL RECEPTORS IN THE RAT ANTERIOR PITUITARY GLAND DURING THE OESTROUS CYCLE: QUANTITATION OF RECEPTOR ACTIVITY IN RELATION TO GONADOTROPHIN RELEASING HORMONE-MEDIATED LUTEINIZING HORMONE RELEASE

1978 ◽  
Vol 76 (2) ◽  
pp. 211-218 ◽  
Author(s):  
K. K. SEN ◽  
K. M. J. MENON
Keyword(s):  
Pituitary Gland ◽  
Binding Sites ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Oestrous Cycle ◽  
Hormone Release ◽  
Releasing Hormone ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Stimulation Of

Specific oestradiol binding to a receptor in nuclear and cytosol fractions of the rat anterior pituitary gland and pituitary responsiveness to gonadotrophin releasing hormone (GnRH) during the oestrous cycle have been studied. To accomplish this, both unoccupied and occupied oestradiol-binding sites in the cytosol and oestradiol-binding sites in the nucleus and total cell were measured during the oestrous cycle. The concentration of unoccupied and occupied sites and total oestradiol binding in the cytosol fluctuated during the cycle. At pro-oestrus, the concentration of cytosol receptor was diminished by about 40% and replenishment occurred during oestrus. On the other hand, a profound increase in concentrations of cellular and nuclear receptors occurred at pro-oestrus. Administration of GnRH significantly stimulated LH release at all stages of the cycle. The maximum stimulation of LH release by GnRH was observed at 13.00 h of pro-oestrus. From these studies, it is concluded that pituitary responsiveness to exogenous GnRH during pro-oestrus parallels the changes in the content of oestrogen receptors in the cytosol and nucleus.

A gonadotrophin-releasing hormone (GnRH) antagonist inhibits GnRH- but not LH-induced meiosis in follicle-enclosed rat oocytes in vitro

1982 ◽  
Vol 101 (2) ◽  
pp. 264-267 ◽  
Author(s):  
C. Ekholm ◽  
T. Hillensjö ◽  
W. J. Le Maire ◽  
C. Magnusson ◽  
C. S. Sheela Rani
Keyword(s):  
Gnrh Agonist ◽  
Gnrh Antagonist ◽  
Similar Response ◽  
Releasing Hormone ◽  
Lactate Accumulation ◽  
Receptor Sites ◽  
Gonadotrophin Releasing Hormone ◽  
Stimulation Of

Abstract. Previous studies have shown that gonadotrophin-releasing hormone (GnRH) can induce resumption of meiosis in follicle-enclosed rat oocytes. In the present study a GnRH antagonistic analogue ([d-pGlul, d-Phe2,-d-Trp3,6]LRF) was found to effectively abolish the stimulatory effect of a GnRH agonist upon resumption of meiosis and lactate accumulation in isolated pre-ovulatory rat follicles but the have no effect on LH stimulation of these parameters. It is concluded that although LH and GnRH can evoke a similar response they act through separate receptor sites and that it is unlikely that GnRH mediates the effect of LH on meiosis or glycolysis.

EFFECT OF VARIOUS PUTATIVE NEUROTRANSMITTERS ON THE SECRETION OF CORTICOTROPHIN-RELEASING HORMONE FROM THE RAT HYPOTHALAMUS IN VITRO – A MODEL OF THE NEUROTRANSMITTERS INVOLVED

1976 ◽  
Vol 69 (1) ◽  
pp. 1-10 ◽  
Author(s):  
M. T. JONES ◽  
E. W. HILLHOUSE ◽  
JANET BURDEN
Keyword(s):  
Median Eminence ◽  
Incubation Medium ◽  
Direct Action ◽  
Aminobutyric Acid ◽  
Male Rats ◽  
Releasing Hormone ◽  
Inhibitory Neurotransmitters ◽  
Basal Release ◽  
Dose Dependent

SUMMARY The effect of incubating the hypothalamus of adult male rats with various neurotransmitters upon the release of corticotrophin-releasing hormone (CRH) was studied. The CRH activity in the incubation medium was assayed in 48 h median eminence-lesioned rats and the corticosteroidogenesis of excised adrenals in vitro was used as the end-point. 5-Hydroxytryptamine (100 pg/ml–10 ng/ml) caused a dose-dependent release of CRH which was antagonized by methysergide (30–100 ng/ml). The response to 5-hydroxytryptamine was also inhibited by hexamethonium and atropine which indicated that it was acting through a cholinergic interneurone. Melatonin (10 ng) did not alter the basal release of CRH but inhibited the action of both 5-hydroxytryptamine (10 ng) and acetylcholine (3 pg). Thus it appears that both 5-hydroxytryptamine and melatonin play a role in the control of CRH release. Noradrenaline blocked the release of CRH induced by both acetylcholine and 5-hydroxytryptamine and presumably this inhibition was caused by direct action on the CRH neurone. γ-Aminobutyric acid (GABA) also inhibited the release of CRH and may also be involved in the regulation of CRH secretion. The inhibitory neurotransmitters, noradrenaline, GABA and melatonin, act via independent receptor mechanisms. A model based on the above data is presented.

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

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.

Circulating gonadotrophin surge-attenuating factor from superovulated women suppresses in vitro gonadotrophin-releasing hormone self-priming

1994 ◽  
Vol 143 (1) ◽  
pp. 45-54 ◽  
Author(s):  
P A Fowler ◽  
P Cunningham ◽  
M Fraser ◽  
F MacGregor ◽  
B Byrne ◽  
...  
Keyword(s):  
Follicular Fluid ◽  
Peripheral Circulation ◽  
Basal Secretion ◽  
Releasing Hormone ◽  
Significant Difference ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Marked Suppression ◽  
Stimulation Of

Abstract A penfusion system based on ovine pituitary tissue explants was used to investigate the effects of follicular fluid (hFF) and serum from superovulated women on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH). The specific aims of the study were to determine both if gonadotrophin surge-attenuating factor (GnSAF) bioactivity is present in the peripheral circulation as well as in the follicles of superovulated women and if GnSAF suppresses GnRH self-priming in vitro. Two pulses of GnRH, 1 h apart, produced marked peaks in LH secreted from control chambers, with GnRH self-priming evident in the significant difference between the first (134·4±1·7–232·1±24·0% of basal secretion) and second (183·9±15·8–313·9±14·0% of basal secretion) LH peaks. Both follicular fluid and serum pooled from two different groups of women produced marked suppression of the first (unprimed) and second (primed) LH peaks. The hFF reduced the first LH peak to 69·6±7·8 and 60·2±9·7% and the second LH peak to 57·4±6·7 and 42·6±6·5% of control LH secretion. Overall, the serum reduced the first and second LH peaks to 76·8±4·2 and 62·9±3·6% of control respectively. These results demonstrated that GnSAF bioactivity suppresses GnRH self-priming, and is present in both the peripheral circulation and hFF. The same material administered to dispersed ovine pituitary monolayers produced similar marked suppression of GnRH-induced LH secretion, with approximately 50-fold less GnSAF bioactivity in serum compared with hFF. Combined doses of oestradiol and progesterone, or hFF from large follicles containing little GnSAF, produced stimulation of GnRH-induced LH secretion and GnRH self-priming (second peaks 78·1±38·9 and 27·4±15·7% respectively higher than first peaks). Thus, in conclusion, GnSAF in hFF and serum markedly attenuated both unprimed and primed pituitary response to GnRH, virtually abolishing the GnRH self-priming effect. Journal of Endocrinology (1994) 143, 45–54

FSH causes a time-dependent stimulation of preovulatory follicle growth in the absence of pulsatile LH secretion in ewes chronically treated with gonadotrophin-releasing hormone agonist

1990 ◽  
Vol 126 (2) ◽  
pp. 297-307 ◽  
Author(s):  
H. M. Picton ◽  
C. G. Tsonis ◽  
A. S. McNeilly
Keyword(s):  
Plasma Concentration ◽  
Gnrh Agonist ◽  
Corpora Lutea ◽  
Preovulatory Follicle ◽  
Follicle Growth ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
The Mean ◽  
Stimulation Of

ABSTRACT The study investigated the relationship between the plasma concentration of FSH and the stimulation of preovulatory follicle growth in vivo in ewes chronically treated with the gonadotrophin-releasing hormone (GnRH) agonist buserelin (HOE 766). Welsh Mountain ewes with regular oestrous cycles were treated for 6 weeks with two discs implants placed s.c., each containing 5 mg of the agonist in a matrix of polyhydroxybutyric acid. Treatment with the agonist for 35 days produced a sustained suppression of the plasma concentration of FSH, stopped the pulsatile release of LH and prevented follicular development beyond 2·5 mm diameter. There was no difference between the total number of follicles > 1·0 mm diameter present in the ovaries of GnRH agonist-treated ewes and day 8 luteal phase control ewes. During the sixth week of agonist treatment ewes were infused with ovine FSH (6 μg NIADDK-oFSH16/h) in the presence of only basal concentrations of LH. After 24, 48, 72 or 120 h of FSH infusion, the mean number of follicles > 1 ·0 mm diameter per ewe was not significantly different between treated and control animals. Infusion of FSH caused a timedependent increase in (1) the number of follicles per ovary >2·5 mm, (2) the mean diameter of these follicles and (3) the proportion of the large follicles which could be classified as oestrogenic (> 3·7 nmol oestradiol/follicle per h in vitro). Injection of human chorionic gonadotrophin (750IU i.m.) after 120 h of FSH infusion caused the majority of these large follicles to ovulate and form apparently normal corpora lutea. These results indicate that, in the absence of pulsatile LH, FSH stimulates the growth of normal large oestrogenic follicles which, when stimulated, ovulate to produce viable corpora lutea. Journal of Endocrinology (1990) 126, 297–307

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