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.

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.

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.

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

Testosterone maintains pituitary and serum FSH and spermatogenesis in gonadotrophin-releasing hormone antagonist-suppressed rats

1986 ◽  
Vol 108 (1) ◽  
pp. 101-107 ◽  
Author(s):  
M. A. Rea ◽  
G. R. Marshall ◽  
G. F. Weinbauer ◽  
E. Nieschlag
Keyword(s):  
Serum Testosterone ◽  
Treated Group ◽  
Male Rats ◽  
Testis Weight ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Hypophysectomized Rats ◽  
Gonadotrophin Releasing Hormone ◽  
Vehicle Treated Control

ABSTRACT Groups of adult male rats were treated continuously for 30 days with either vehicle or the potent gonadotrophin-releasing hormone (GnRH) antagonist, (N-Ac-d-Nal(2)1,d-pCl-Phe2,d-Trp3,d-hArg (Et2)6,d-Ala10)-GnRH (RS 68439; 35 μg/day). In addition, groups of vehicle- and antagonist-treated rats received s.c. testosterone implants sufficient to maintain serum testosterone concentrations 3·5- to 5-fold higher than those of vehicle-treated control rats. After 30 days of antagonist treatment serum LH, FSH and testosterone concentrations were at or below the detection limits of their respective assays and pituitary FSH content and GnRH receptor binding were reduced, relative to control animals, by 77 and 98% respectively. Testis weight in antagonist-treated rats was reduced by 75% and spermatogenesis was suppressed to an extent comparable to that observed in hypophysectomized rats. Testosterone, which caused a 40% reduction in serum FSH relative to control animals, prevented the antagonist-induced fall in both serum and pituitary FSH, but not GnRH receptors, below that observed in the vehicle plus testosterone-treated group. Furthermore, spermatogenesis in the antagonist plus testosterone-treated group was indistinguishable from that observed in control animals. It is concluded that testosterone is capable of maintaining serum and pituitary FSH levels in vivo, under conditions which presumably render the pituitary insensitive to hypothalamic GnRH. J. Endocr. (1986) 108, 101–107

RESPONSE OF THE PITUITARY-TESTICULAR AXIS TO LUTEINIZING HORMONE-RELEASING HORMONE IN THE IMMATURE MALE RAT

1977 ◽  
Vol 84 (2) ◽  
pp. 254-267 ◽  
Author(s):  
H. Edward Grotjan ◽  
Donald C. Johnson
Keyword(s):  
Luteinizing Hormone ◽  
Control Level ◽  
Serum Testosterone ◽  
Male Rats ◽  
Male Rat ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Immature Male ◽  
Serum Lh ◽  
Lh Rh

ABSTRACT Follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone and androstenedione were measured by radioimmunoassays in the sera of immature male rats treated with luteinizing hormone-releasing hormone (LH-RH). A single dose of 10, 20, 40 or 80 ng of LH-RH produced a prompt increase in serum LH: significant changes in FSH were found only with the two larger doses. Serum testosterone increased to peak levels in 20 to 40 min and returned to control level by 120 min. Changes in androstenedione were temporally similar but smaller in magnitude. Four doses of 20 or 40 ng LH-RH given at 20 min intervals did not increase serum LH or testosterone concentrations above those found with a single injection; FSH was slightly higher after the fourth dose. However, 40 ng LH-RH given every 20 min for 2 h produced a dramatic increase in serum LH and FSH: serum and testicular androgens were also much higher during the second hour. A 2 h stimulation with 80 ng LH-RH given ip at 30 min intervals did not alter the response to the same treatment given 24 h later; i. e., neither the pituitary nor the gonad was primed by previous exposure to increased levels of LH-RH or gonadotrophins. These results suggest that a single pulse of LH-RH produces a predictable response in the animal, but multiple episodic stimuli produce variable responses: testes, on the other hand, produce androgens as long as gonadotrophins are available.

Influence of the environmental temperature on the post-partum testosterone surge in the rat

1987 ◽  
Vol 115 (4) ◽  
pp. 478-482 ◽  
Author(s):  
J. Roffi ◽  
F. Chami ◽  
P. Corbier ◽  
D. A. Edwards
Keyword(s):  
Ambient Temperature ◽  
Environmental Temperature ◽  
Post Partum ◽  
Serum Testosterone ◽  
The Body ◽  
Male Rats ◽  
Effect Of Temperature ◽  
Male Rat ◽  
Foster Mother ◽  
The Central Nervous System

Abstract. In the neonatal male rat, a rapid and transient increase in serum testosterone occurs about 2 h after birth. This post-partum testosterone surge (PPTS) has been implicated in the masculinization and defeminization of the central nervous system. The present study shows that environmental temperature can have a profound influence on the PPTS. Male rats were delivered from their mothers by caesarean section on day 22 of gestation. Immediately thereafter, neonatal males were placed at an ambient temperature of either 18, 21, 24 or 30°C. With 2 h of exposure, the body temperature was in close correspondence with the ambient temperature. The PPTS was clearly abolished in the pups exposed for 2 h at either 18 or 21°C. The effect of temperature was reversible: by placing pups at either 18 or 21°C for 2 h after delivery, and then rewarming by placing them with a foster mother, the PPTS was delayed until 4 h after birth, i.e. 2 h after the beginning of rewarming. Thus, environmental cooling appears to retard the development of neural and/or endocrine systems mediating the PPTS. Aberrant maternal care which would produce substantial cooling of the male pups would be expected to affect the PPTS, which in turn might affect the sexuality of male progeny.

HYPOTHALAMIC, PITUITARY AND TESTICULAR FUNCTION DURING SEXUAL MATURATION OF THE MALE RAT

1977 ◽  
Vol 72 (1) ◽  
pp. 17-26 ◽  
Author(s):  
A. H. PAYNE ◽  
R. P. KELCH ◽  
E. P. MURONO ◽  
J. T. KERLAN
Keyword(s):  
Dehydrogenase Activity ◽  
Sexual Maturation ◽  
Hydroxysteroid Dehydrogenase ◽  
Male Rat ◽  
Releasing Hormone ◽  
Isomerase Activity ◽  
Serum Lh ◽  
Rate Of Increase ◽  
Gonadotrophin Releasing Hormone

SUMMARY Hypothalamic content of gonadotrophin-releasing hormone (GnRH), serum LH and FSH, capacity of the testis to synthesize testosterone in vitro, and testicular 5-ene-3β-hydroxysteroid dehydrogenase-isomerase and 17β-hydroxysteroid dehydrogenase were measured in groups of rats at approximately 5 day intervals from birth to day 64 and at days 74 and 89. The capacity of the testes to synthesize testosterone in vitro was measured in the presence of a saturating dose of rat LH. Gonadotrophin-releasing hormone increased steadily from 0·17 ng per hypothalamus at birth to a maximum of 7 ng at day 52 and then remained constant. LH concentrations were highly variable and often exceeded adult values between days 10 and 32. After day 32 a steady rise was observed which reached adult values between days 37 and 42. FSH concentrations markedly increased from 255 ng/ml observed at birth and day 10 to a peak value of 1000 ng/ml at day 32. Subsequently there was a steady decline in FSH values until day 74 when the concentration returned to values found at birth. 5-ene-3β-Hydroxysteroid dehydrogenase-isomerase activity exhibited a rapid increase between days 12 and 19 followed by an even greater rate of increase between days 19 and 32 when adult levels were attained. 17β-Hydroxysteroid dehydrogenase activity was very low between birth and day 22. Enzyme activity began to increase at day 22 with a rapid increase in activity observed between days 37 and 58. The increase in capacity to synthesize testosterone closely followed the increase in 17β-hydroxysteroid dehydrogenase activity. The study demonstrates that during sexual maturation in the male rat, changes in serum LH and FSH do not reflect changes in hypothalamic GnRH. The appearance of Leydig cells as monitored by 5-ene-3β-hydroxysteroid dehydrogenase-isomerase activity precedes by approximately 20 days the increase in testicular capacity to synthesize testosterone in vitro. The latter coincides with the increase in 17β-hydroxysteroid dehydrogenase activity. These results suggest that 17β-hydroxysteroid dehydrogenase is a limiting factor in the ability of the testis to respond to LH stimulation.

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