Effect of Intermittent Infusion of LH-Releasing Hormone on Serum LH and FSH Levels In Immature Male Rats

1975 ◽  
Vol 148 (3) ◽  
pp. 913-917 ◽  
Author(s):  
J. A. Vilchez-Martinez ◽  
A. Arimura ◽  
A. V. Schally
Keyword(s):  
Intermittent Infusion ◽  
Male Rats ◽  
Releasing Hormone ◽  
Immature Male ◽  
Serum Lh ◽  
Lh Releasing Hormone

Testosterone metabolites do not participate in the control of hypothalamic LH-releasing hormone

1986 ◽  
Vol 109 (2) ◽  
pp. 291-296 ◽  
Author(s):  
M. Zanisi ◽  
F. Celotti ◽  
P. Ferraboschi ◽  
M. Motta
Keyword(s):  
Testosterone Propionate ◽  
Male Rats ◽  
Free Form ◽  
Releasing Hormone ◽  
Specific Radioimmunoassay ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Testosterone Metabolites ◽  
Lh Releasing Hormone

ABSTRACT To determine whether the ability of testosterone to increase intrahypothalamic LH-releasing hormone (LHRH) in orchidectomized rats might be explained by the conversion of the hormone into either its 5α-reduced or oestrogenic metabolites, testosterone, 5α-androstan-17β-ol-3-one (DHT), 5α-androstane-3α, 17β-diol (3α-diol) and 5α-androstane-3β,17β-diol (3β-diol) (2 mg/rat per day for 6 days) and oestradiol (0·1, 0·5, 1·0 and 5·0 μg/rat per day for 6 days) were injected into castrated male rats. After 6 days the rats were killed and serum LH levels and intrahypothalamic LHRH stores measured using specific radioimmunoassay procedures. Testosterone and its 5α-reduced metabolites were used in either the free alcohol or the propionate form (dipropionates in the case of the diols); oestradiol was used as oestradiol-17β or in the benzoate form. Treatment with testosterone, DHT, 3α-diol and 3β-diol resulted in a significant decrease in serum LH levels; all the 5α-reduced testosterone derivatives were more effective than testosterone in this respect. Testosterone and DHT propionates suppressed LH release following orchidectomy totally; 3α-diol and 3β-diol dipropionates were less effective. Testosterone increased intrahypothalamic LHRH stores, this effect being much higher after testosterone propionate, i.e. when intrahypothalamic LHRH stores were restored to pre-castration levels. None of the 5α-reduced steroids was capable of modifying the low intrahypothalamic levels of LHRH found following orchidectomy; only 3α-diol dipropionate exhibited some activity, but this was much lower than that of testosterone propionate. Oestradiol-17β was totally ineffective in decreasing serum LH in orchidectomized animals; in contrast, oestradiol benzoate progressively decreased serum LH. Oestradiol in the free form was unable to increase LHRH stores, as was oestradiol benzoate except at the highest dose. The results suggest that the effect exerted by testosterone on hypothalamic LHRH is due to the hormone as such and does not involve its conversion into either 5α-reduced or oestrogenic metabolites. J. Endocr. (1986) 109, 291–296

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

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.

LUTEINIZING HORMONE RELEASING HORMONE-INDUCED RELEASE OF LUTEINIZING HORMONE FROM PITUITARY EXPLANTS OF COWS KILLED BEFORE OR AFTER OESTRADIOL TREATMENT

1981 ◽  
Vol 88 (1) ◽  
pp. 17-25 ◽  
Author(s):  
E. M. CONVEY ◽  
J. S. KESNER ◽  
V. PADMANABHAN ◽  
T. D. CARRUTHERS ◽  
T. W. BECK
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Oestradiol Treatment ◽  
Readily Releasable Pool ◽  
Serum Lh ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Releasing Hormone

In ovariectomized heifers, oestradiol decreases concentrations of LH in serum for approximately 12 h after which LH is released in a surge comparable in size and duration to the preovulatory surge. Using this model, we measured LH release induced by LH releasing hormone (LH-RH) from pituitary explants taken from ovariectomized heifers before or after an oestradiol-induced LH surge. These changes were related to changes in LH concentrations in serum and pituitary glands and hypothalamic LH-RH content. Twenty Holstein heifers were randomly assigned to one of four treatment groups to be killed 0, 6, 12, or 24 h after the injection of 500 μg oestradiol-17β. Jugular blood was collected at −2, −1 and 0 h then at intervals of 2 h until slaughter. Pituitary glands were collected and ≃2 mm3 explants were exposed to 4 ng LH-RH/ml medium for 30 min (superfusion) or 4 ng LH-RH/ml medium for 2 h in Erlenmeyer flasks. Levels of LH were measured in the medium. Hypothalami, collected at autopsy, were assayed for LH-RH content. To determine pituitary LH content, an additional 15 ovariectomized heifers were killed, five each at 0, 12 and 24 h after the injection of 500 μg oestradiol. In both groups of heifers, oestradiol reduced serum LH concentrations to ≃ 1 ng/ml, a level which persisted for 12 h, when LH was released in a surge. Pituitary sensitivity to LH-RH was increased at 6 and 12 h after the injection of oestradiol, but was markedly decreased at 24 h, i.e. after the LH surge. Despite this twofold increase in capacity of the pituitary gland to release LH in response to LH-RH, pituitary LH content did not change during 12 h after oestradiol treatment. However, LH content decreased after the LH surge and this decrease was associated with a decrease in pituitary responsiveness to LH-RH. Hypothalamic LH-RH content was not altered by these treatments. We have interpreted our results as evidence that oestradiol exerts a positive feedback effect on the pituitary gland of ovariectomized heifers such that pituitary sensitivity to LH-RH is increased twofold by the time the LH surge is initiated. In addition, oestradiol causes a transitory inhibition of LH-RH release as shown by the fact that serum LH concentrations remained low during the interval from injection of oestradiol until the beginning of the LH surge despite the fact that pituitary sensitivity to LH-RH is increased at this time. Depletion of a readily releasable pool of pituitary LH may be the mechanism by which the LH surge is terminated.

Changes in pituitary responsiveness to LH-releasing hormone after acute buserelin treatment: a time-course and dose–response study

1985 ◽  
Vol 106 (1) ◽  
pp. 27-30 ◽  
Author(s):  
J. D. Heather ◽  
S. A. Whitehead
Keyword(s):  
Time Course ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Significant Difference ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
In Vivo Effects ◽  
Dose Response Study

ABSTRACT The acute in-vivo effects of a potent LH-releasing hormone (LHRH) agonist, buserelin, on LH secretion and pituitary responsiveness to LHRH have been investigated in oestrous rats. Doses of 50, 100 and 250 ng buserelin stimulated LH release in a dose-dependent manner, the peak serum LH concentrations being measured 1 h after the treatment. Thereafter LH levels fell rapidly between 1 and 6 h and by 18 h serum LH concentrations were similar in all groups of animals. Pituitary responsiveness to a challenge with 100 ng LHRH was potentiated by 50 or 100 ng buserelin injected 1 or 2 h before the LHRH challenge. In contrast, 250 ng buserelin completely abolished the LH response to LHRH when tested 1, 2 and 4 h after treatment, but by 6 h a small but attenuated response was observed. Four hours after treatment there was no significant difference in the responses when compared with the saline-treated controls. J. Endocr. (1985) 106, 27–30

Effects on growth and body composition of androgen deprivation by castration or autoimmunization to LH-releasing hormone in the male rat under conditions of controlled food intake

1986 ◽  
Vol 110 (1) ◽  
pp. 97-102 ◽  
Author(s):  
J. M. Fletcher ◽  
G. E. Lobley ◽  
A. Connell
Keyword(s):  
Body Composition ◽  
Food Intake ◽  
Gonadal Hormones ◽  
Female Rats ◽  
Male Rats ◽  
Releasing Hormone ◽  
Energy Retention ◽  
Lh Releasing Hormone ◽  
Testicular Steroids ◽  
Intact Rats

ABSTRACT The effects of endogenous gonadal hormones on the regulation of body composition and energy retention have been investigated under conditions of controlled food intake. Male and female rats were fed the same amount from weaning to 82 days of age. The carcases of males contained more protein, less lipid and yielded more ash than females, but they had the same amount of total energy in their carcases as females. In a second experiment, male rats were sham-operated or castrated at 19 days and then fed equal amounts from weaning. At 40 days, intact and castrated rats did not differ in total carcase energy content nor in carcase composition. At 82 days the carcases of intact rats had more protein but had retained the same amount of energy as castrated rats. By 131 days, the difference in protein content was larger and intact rats had less carcase lipid, less carcase energy and gave less ash than castrated rats. At the same age and with a similar food intake, the differences in carcase composition between intact males and females were considerably larger than between intact and castrated males. In a third experiment, male rats were sham-operated or castrated at 1 day post partum and fed the same amount as in the second experiment from weaning to 82 days. Both sham-castrated and castrated rats grew less well than rats operated on at 19 days. The differences in carcase composition between intact and castrated rats were in the same direction but of greater magnitude than in rats operated at the later age. In a fourth experiment the effects on body compositon and energy retention of sham-operation, castration or immunization to LH-releasing hormone (LHRH) at weaning were compared in male rats fed the same amount from weaning to 131 days. Intact rats retained less carcase energy, less lipid and produced less ash than castrated and LHRH-immunized animals. Castrated and LHRH-immunized rats did not differ in carcase composition or amount of energy retained. It is concluded that (1) endogenous sex steroids affect growth and carcase composition independently of food intake, (2) the characteristic carcase composition of the female rat is largely due to the presence of ovarian steroids rather than lack of testicular steroids, (3) in the absence of increased food intake the effects of testicular steroids upon growth and energy expenditure are small but similar to those found in animals with free access to food, (4) the long-terms effects of perinatal exposure to testicular steroids upon growth and carcase composition are not only a consequence of changed food intake and (5) surgical castration and functional castration, induced by LHRH auto-immunization, produce the same effects on carcase composition. J. Endocr. (1986) 110, 97–102

EFFECT OF ACTINOMYCIN D ON THE PITUITARY RESPONSE TO LH-RH

1976 ◽  
Vol 81 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Jesus A. Vilchez-Martinez ◽  
Akira Arimura ◽  
Andrew V. Schally
Keyword(s):  
Initial Phase ◽  
Rna Synthesis ◽  
Actinomycin D ◽  
Male Rats ◽  
Continuous Stimulation ◽  
Immature Male ◽  
Serum Lh ◽  
Pre Treatment ◽  
Lh Rh

ABSTRACT The effect of Actinomycin D (Act D) on the release of LH and FSH induced by LH-RH was investigated in rats. Immature male rats received an iv infusion over a period of 3–4 h or a quick iv injection of synthetic LH-RH. Infusion of LH-RH significantly increased serum LH and FSH levels at 1, 2, 3 and 4 h after the initiation of infusion. Pre-treatment with 100 μg/100 g b. w. Act D failed to affect the rise of serum LH and FSH levels 1 h after the infusion but significantly suppressed the response at 2, 3 and 4 h. The increase in serum LH and FSH levels after a quick injection of LH-RH was unaffected by pre-treatment with Act D whether the antibiotic was injected 1 or 2 h before LH-RH. The results suggest that the initial phase of the pituitary response to LH-RH does not require DNA-dependent RNA synthesis, whereas that in the later period does. RNA synthesis may be necessary only to maintain the increased secretion of both LH and FSH during a continuous stimulation with LH-RH.

227 AN ALTERATION IN GENE EXPRESSION PATTERNS INDUCED BY DI-(2 ETHYLHEXYL) PHTHALATE AND FLUTAMIDE IN THE TESTIS OF IMMATURE MALE RATS

2009 ◽  
Vol 21 (1) ◽  
pp. 211
Author(s):  
K.-C. Choi ◽  
T. T. B. Vo ◽  
E.-M. Jung ◽  
V. H. Dang ◽  
E.-B. Jeung
Keyword(s):  
Gene Expression ◽  
Reproductive System ◽  
Male Reproductive System ◽  
Male Rats ◽  
Calcium Signal ◽  
High Dose ◽  
Dependent Manner ◽  
Immature Male ◽  
Serum Lh ◽  
Ethylhexyl Phthalate

In a previous study, we demonstrated that although endocrine disruptors (EDs) with androgenic and anti-androgenic effects may alter reproductive function, their effects on the developing male reproductive organs may be distinct. To continue this line of study, we treated immature rats to examine the adverse effects of di-(2 ethylhexyl) phthalate (DEHP) and flutamide (Flu) on the male reproductive system. Immature male SD rats were treated daily with DEHP and/or Flu at postnatal day (PND) 21 to 35 in a dose-dependent manner, and the changes evoked by these EDs were determined by differences in male reproductive tract and other organ weights, testicular histology, and serum LH and testosterone levels in combination with global microarray analysis. Interestingly, the testes, prostate, seminal vesicle weight, and anogenital distances were significantly decreased in response to the highest dose of DEHP and Flu. There were no differences in serum LH and testosterone concentration at PND 35 for immature male rats exposed to DEHP and/or Flu. However, treatment with DEHP and/or Flu caused histopathological changes in testes in which the degeneration and denseness of germ cells and/or dilatation of the tubular lumen were observed in response to the high dose [500 mg kg–1 of body weight (BW)] of DEHP and medium dose (10 mg kg–1 of BW) of Flu. Additionally, the results from cDNA microarray indicated that 1272 genes were up-regulated (more than 2-fold) and 1969 genes were down-regulated in response to DEPH and/or Flu. These genes were identified based on their roles in some physiological processes (i.e. lipid and cholesterol homeostasis, steroidogenesis, sex determination, and calcium signal transduction). The significant decreases were observed in the expressions of steroidogenic genes (i.e. Star, Cyp11a1, or Hsd3b). In addition, a common set of targeting genes, including CaBP1, Vav2, Plcd1, Lhx1, and Isoc1, were altered following EDs exposure, suggesting a potential set of biomarker genes for screening anti-androgenic and/or androgenicity of EDs. Taken together, we demonstrated that exposure to DEHP and/or Flu resulted in a temporal alteration in gene expression profile in the testes of immature male rats, and their toxicological effects on male reproductive system are distinct depending on their anti-androgenicity, suggesting new insight into molecular mechanism(s) underlying detrimental impacts of EDs with anti-androgenic activities in human and wildlife.

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.

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