Effects of hyperprolactinaemia and testosterone on the release of LH-releasing hormone and the gonadotrophins in intact and castrated rats

1985 ◽  
Vol 104 (1) ◽  
pp. 35-43 ◽  
Author(s):  
A. K. Brar ◽  
A. S. McNeilly ◽  
G. Fink
Keyword(s):  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Pituitary Stalk ◽  
Male Rat ◽  
Female Rat ◽  
Kidney Capsule ◽  
Releasing Hormone ◽  
Gonadotrophin Secretion ◽  
Lh Releasing Hormone

ABSTRACT We have investigated the effect of hyperprolactinaemia on the secretion of LH-releasing hormone (LHRH), LH and FSH in male rats of the PVG strain which were left intact, castrated or castrated and then implanted with either a 10 or 30 mm silicone elastomer capsule containing testosterone (T10 and T30 respectively). Hyperprolactinaemia was produced by pituitary grafts under the kidney capsule. Pituitary stalk blood, for LHRH estimation, and peripheral blood, for LH, FSH and prolactin, were collected under alphaxalone anaesthesia. Pituitary stalk blood was collected during three consecutive periods of 30 min each before, during and after the application of an electrical stimulus to the median eminence (ME). Hyperprolactinaemia significantly reduced the plasma concentrations of FSH in intact rats and the post-castration increase in the plasma concentrations of both LH and FSH. Neither hyperprolactinaemia nor castration had any significant effect on the spontaneous output of LHRH, but castration alone or castration plus implantation of a T30 capsule did significantly reduce the increment in LHRH output produced by ME stimulation, an effect not seen in rats bearing pituitary grafts. The T30, but not the T10 capsules suppressed the post-castration increase in the gonadotrophins, and the inhibitory effect of testosterone was not significantly affected by hyperprolactinaemia. An incidental but important finding was that the presence of pituitary grafts under the kidney capsule reduced the anaesthetic dose of alphaxalone by 63%. These results show that (i) in the male rat the inhibitory effect of hyperprolactinaemia on gonadotrophin secretion is not due to a decrease in the spontaneous release of LHRH, (ii) in contrast to the female rat the post-castration increase in gonadotrophin secretion is not accompanied by an increase in the output of LHRH, (iii) the output of LHRH in response to ME stimulation is affected by castration and testosterone but not by hyperprolactinaemia and (iv) the anaesthetic effects of alphaxalone are potentiated by hyperprolactinaemia, and this may explain in part the potentiation of alphaxalone anaesthesia by oestrogen. J. Endocr. (1985) 104, 35–43

EFFECT OF ADRENALECTOMY OR CASTRATION ON THE INHIBITION OF GONADOTROPHIN SECRETION INDUCED BY HYPERPROLACTINAEMIA IN THE ADULT MALE RAT

1980 ◽  
Vol 85 (1) ◽  
pp. 83-92 ◽  
Author(s):  
A. S. McNEILLY ◽  
R. M. SHARPE ◽  
H. M. FRASER
Keyword(s):  
Adult Male ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Male Rat ◽  
Gonadotrophin Secretion ◽  
Adult Male Rat ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Releasing Hormone

SUMMARY To investigate the role of adrenal and gonadal steroids in the long-term suppression of gonadotrophin secretion induced by prolactin the effects of adrenalectomy or castration on the serum and pituitary levels of LH, FSH and prolactin and the hypothalamic content of LH releasing hormone (LH-RH) have been studied in adult male rats with hyper prolactinaemia produced by the transplantation of pituitary glands under the kidney capsule. Levels of LH and FSH in serum were significantly suppressed in all intact pituitary-grafted rats. Adrenalectomy on the day of pituitary implantation or 20 days later did not affect this suppression. However, castration on days 0,28 or 49 after pituitary grafting resulted in a rise in levels of FSH in serum indistinguishable from that in control rats. While the rise in levels of LH after castration on day 0 was the same as the controls, this increase was significantly reduced 2 days after castration on days 28 and 49 after pituitary grafting. Castration resulted in an increase in the pituitary content of LH and a reduction in the hypothalamic content of LH-RH but no change in the pituitary content of FSH. Hyperprolactinaemia did not appear to affect these responses. The present results showed clearly that the gonad but not the adrenal must be present for prolactin to exert an inhibitory effect on gonadotrophin secretion.

Pituitary-testis function in rats treated neonatally with a gonadotrophin-releasing hormone agonist: short- and long-term effects

1992 ◽  
Vol 134 (2) ◽  
pp. 269-NP ◽  
Author(s):  
P. Garnelo ◽  
L. Pinilla ◽  
F. Gaytan ◽  
E. Aguilar
Keyword(s):  
Plasma Concentrations ◽  
Reproductive Activity ◽  
Male Rats ◽  
Testis Weight ◽  
Long Term Effects ◽  
Releasing Hormone ◽  
Testicular Weight ◽  
Lh Releasing Hormone

ABSTRACT Acute and long-term effects of neonatal and prepubertal treatments with an LH-releasing hormone agonist (LHRH-A) were studied in Wistar male rats. Animals injected with d-Ala6-d-Gly10-LHRH ethylamide (2 μg/kg per day) or vehicle from days 1 to 15 or from days 16 to 29 were killed at different ages. Treatment between days 1 and 15 induced a decrease in both pituitary FSH and LH content as well as a reduction in plasma FSH and blockade of the response to LHRH. These effects were apparent on day 16 after treatment. Basal and human chorionic gonadotrophin (hCG)-stimulated progesterone and testosterone secretion in vitro was similar in testes from male rats treated with LHRH-A or vehicle. Reduced testicular weight was observed until day 90, whereas puberty, spermatogenesis and fertility were unaffected. The decrease in plasma FSH concentrations after neonatal treatment with LHRH-A was also found in groups of animals killed on day 10 and was possibly the cause of reduced testicular weight, since treatment with FSH from day 1 to day 15 blocked the effect of LHRH-A. Likewise, treatment with LHRH-A from day 1 to day 15 also reduced FSH and LH secretion in males orchidectomized on day 1 of life. Animals injected with LHRH-A from day 15 to day 29 exhibited, at the end of the treatment period, reduced testicular weight, and decreased pituitary gonadotrophin content and plasma FSH concentrations, whereas LH plasma concentrations were normal. In adulthood, the pituitary-testis function did not vary from normal. Our results demonstrate that: (1) administration of LHRH-A from day 1 to day 15 of life desensitized the gonadotrophs, which in turn lowered plasma gonadotrophin concentrations and caused a long-term reduction in testis weight without changes in the quality of spermatogenesis or reproductive activity in adulthood; (2) chronic treatment with LHRH-A during the neonatal period did not result in a steroidogenic lesion; and (3) administration of LHRH-A from day 15 to day 29 produced only a transient reduction in testicular weight and in spermatogenesis. Journal of Endocrinology (1992) 134, 269–277

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

Role of LHRH in the gonadotrophin response to restraint stress in intact male rats

1990 ◽  
Vol 124 (2) ◽  
pp. 241-246 ◽  
Author(s):  
A. López-Calderón ◽  
M. I. Gonzaléz-Quijano ◽  
J. A. F. Tresguerres ◽  
C. Ariznavarreta
Keyword(s):  
Chronic Stress ◽  
Negative Correlation ◽  
Restraint Stress ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Intact Male ◽  
Gonadotrophin Secretion ◽  
Site Of Action

ABSTRACT A hypothalamic site of action has been hypothesized for the inhibitory effect of chronic stress on gonadotrophin secretion. The aim of the present study was to examine the temporal changes in hypothalamic LHRH content and gonadotrophin secretion during restraint stress, and the pituitary responsiveness to LHRH stimulation in chronically stressed rats. Adult male rats were killed after being restrained for 0, 20, 45, 90, 180 and 360 min or for 6 h daily over 2, 3 and 4 days. After 20–45 min of stress there was an increase in plasma concentrations of LH (P<0·01) and a decrease in hypothalamic LHRH content (P<0·01), suggesting a negative correlation between plasma LH and hypothalamic LHRH concentrations. Plasma concentrations of FSH were also increased by restraint, but the FSH response was slower and less than the plasma LH response, being significant after 90 min of restraint. Plasma LH and FSH and hypothalamic LHRH concentrations were decreased in chronically stressed rats. In rats restrained for 6 h daily over 4 days, the response of plasma gonadotrophins to administration of 500 ng LHRH was enhanced 45 min after the injection. On the basis of these observations we concluded that in the intact rat, stress may acutely stimulate LHRH and gonadotrophin secretion, and the inhibitory effect of chronic stress on plasma LH and FSH seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a decrease in LHRH secretion. Journal of Endocrinology (1990) 124, 241–246

Hypothalamic-pituitary function in neonatally oestrogen-treated male rats

1992 ◽  
Vol 134 (2) ◽  
pp. 279-NP ◽  
Author(s):  
L. Pinilla ◽  
P. Garnelo ◽  
F. Gaytan ◽  
E. Aguilar
Keyword(s):  
Olive Oil ◽  
Plasma Concentrations ◽  
Male Rats ◽  
Lhrh Agonist ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Lh Releasing Hormone ◽  
Wistar Male Rats

ABSTRACT Neonatal oestrogen administration to male rats permanently impaired the function of the pituitary-testicular axis possibly by inhibiting neonatal gonadotrophin secretion. To analyse the hypothalamus and/or pituitary involvement in this inhibition, pituitary responsiveness to acute stimulation with LH-releasing hormone (LHRH) was studied in vivo and in vitro in Wistar male rats injected on day 1 of age with oestradiol benzoate (OB) or olive oil. FSH and LH pituitary content and plasma concentrations were reduced in oestrogenized male rats at days 10 and 16 of age. Likewise, the in-vivo increase in gonadotrophin plasma concentrations after acute stimulation with LHRH was almost completely suppressed in 10-and 16-day-old oestrogenized males. In vitro, the increased secretion of FSH after LHRH stimulation was abolished and the LH response strongly reduced in pituitaries from oestrogenized males. Finally, the effects of neonatal oestrogenization were not abolished by treatment from day 1 to day 15 with an LHRH agonist (0·01 μg/kg per 12 h). We conclude that in male rats the effects of oestrogenization are due to both a reduction in LHRH endogenous secretion and a decrease in the pituitary responsiveness to LHRH. Journal of Endocrinology (1992) 134, 279–286

USE OF A PULSED INFUSION OF LUTEINIZING HORMONE RELEASING HORMONE TO MIMIC SEASONALLY INDUCED ENDOCRINE CHANGES IN THE RAM

1979 ◽  
Vol 83 (2) ◽  
pp. 251-260 ◽  
Author(s):  
G. A. LINCOLN
Keyword(s):  
Plasma Concentrations ◽  
Prolonged Treatment ◽  
Mating Season ◽  
Releasing Hormone ◽  
Natural Lighting ◽  
Sexual Skin ◽  
Gonadotrophin Secretion ◽  
The Individual ◽  
Lh Rh ◽  
Lh Releasing Hormone

Adult Soay rams were housed indoors under natural lighting during the spring non-mating season when gonadotrophin secretion was low. Four animals received small doses (100 ng or 500 ng) of synthetic LH releasing hormone (LH-RH) infused into the jugular vein by a mechanical device for 60 s every 2 h for 33–57 days: two other rams acted as controls. The prolonged treatment with LH-RH resulted in growth of the testes and the development of the sexual skin flush; these effects were lost when treatment stopped. The plasma concentrations of LH, FSH and testosterone were low at the beginning; each short infusion of LH-RH resulted in a transitory increase in the level of LH and testosterone while the concentration of FSH was only marginally affected. After prolonged treatment with 500 ng pulses of LH-RH the plasma concentrations of all three hormones were permanently raised. The response to the individual injections of LH-RH was also modified, the peak in LH being reduced in amplitude but more prolonged while the FSH and testosterone responses were both enhanced. When the pulsed infusion was stopped the concentration of LH and testosterone declined rapidly while the decline in FSH levels took many days. These endocrine changes induced by the pulsed infusion are comparable to those that occur naturally in the ram during testicular redevelopment before the mating season.

Certain aspects of the host-parasite relationship ofNematospiroides dubius(Baylis). II. The effect of sex on experimental infections in the rat (an abnormal host)

Parasitology ◽  
1961 ◽  
Vol 51 (3-4) ◽  
pp. 499-510 ◽  
Author(s):  
Colin Dobson
Keyword(s):  
Male Rats ◽  
Male Rat ◽  
Normal Male ◽  
Female Rat ◽  
Castrate Male ◽  
Parasite Relationship ◽  
Nematospiroides Dubius ◽  
Resistance To Infection ◽  
Host Parasite ◽  
The Relationship

1. The male rat is more susceptible to infections ofNematospiroides dubiusthan the female. As the rat grows older the resistance of the female rat to infection increases at a greater rate than that of the male.2. The course of the infection is modified by the sex of the host.3. More larvae penetrated the intestinal mucosa to encyst in the male than in the female. More larvae, however, formed cysts in the female than in the male rat by the fifth day.4. The male harboured more adult worms than the female rat, although this difference was not significant in the immature animals.5. The sex resistance of the rat toN. dubiusinfections was removed by bilateral gonadectomy. Castration decreased the susceptibility of the male rat, while spaying increased it in the female compared with the susceptibility in the respective normal hosts.6. Subsequent replacement of the homologous sex hormone in the gonadectomized rat restores the sex resistance, and may even increase it (particularly in the immature animals). Oestradiol increased the resistance of the spayed female rat, while testosterone increased the susceptibility of the castrate male rat to infection.7. Oestradiol implanted in castrate male rats increased the resistance of these hosts to a greater level than was shown in the normal male rat.8. The rat shows a marked age resistance over which the sex resistance is superimposed.9. The relationship between the sex of the host and its resistance to infection is discussed.This work was done during the tenure of a Department of Scientific and Industrial Research Studentship. My thanks are due to Dr E. T. B. Francis for his helpful and critical supervision and to Professor I. Chester Jones, in whose department the work was done, for the facilities he provided.

scholarly journals Increased bioactivation of dihaloalkanes in rat liver due to induction of class Theta glutathione S-transferase T1-1

1998 ◽  
Vol 335 (3) ◽  
pp. 619-630 ◽  
Author(s):  
Philip J. SHERRATT ◽  
Margaret M. MANSON ◽  
Anne M. THOMSON ◽  
Erna A. M. HISSINK ◽  
Gordon E. NEAL ◽  
...  
Keyword(s):  
Western Blotting ◽  
Rat Liver ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Female Rat ◽  
Glutathione S Transferase ◽  
Chemopreventive Agents ◽  
Cytoplasmic Staining ◽  
Potent Inducer

A characteristic feature of the class Theta glutathione S-transferase (GST) T1-1 is its ability to activate dichloromethane and dibromoethane by catalysing the formation of mutagenic conjugates. The level of the GSTT1 subunit within tissues is an important determinant of susceptibility to the carcinogenic effects of these dihaloalkanes. In the present study it is demonstrated that hepatic GST activity towards these compounds can be elevated significantly in female and male Fischer-344 rats by feeding these animals on diets supplemented with cancer chemopreventive agents. Immunoblotting experiments showed that increased activity towards the dihaloalkanes is associated with elevated levels of the GSTT1 subunit in rat liver. Sex-specific effects were observed in the induction of GSTT1 protein. Amongst the chemopreventive agents tested, indole-3-carbinol proved to be the most potent inducer of hepatic GSTT1 in male rats (6.2-fold), whereas coumarin was the most potent inducer of this subunit in the livers of female rats (3.5-fold). Phenobarbital showed significant induction of GSTT1 only in male rat liver and had little effect in female rat liver. Western blotting showed that class Alpha, Mu and Pi GST subunits are not co-ordinately induced with GSTT1, indicating that the expression of GSTT1 is determined, at least in part, by mechanisms distinct from those that regulate levels of other transferases. The increase in amount of hepatic GSTT1 protein was also reflected by an increase in the steady-state level of mRNA in response to treatment with chemopreventive agents and model inducers. Immunohistochemical detection of GSTT1 in rat liver supported the Western blotting data, but showed, in addition to cytoplasmic staining, significant nuclear localization of the enzyme in hepatocytes from some treated animals, including those fed on an oltipraz-containing diet. Significantly, the hepatic level of cytochrome P-450 2E1, an enzyme which offers a detoxification pathway for dihaloalkanes, was unchanged by the various inducing agents studied. It is concluded that the induction of GSTT1 by dietary components and its localization within cells are important factors that should be considered when assessing the risk dihaloalkanes pose to human health.

Regulation of CRH-induced secretion of ACTH and corticosterone by SOM230 in rats

2005 ◽  
Vol 153 (3) ◽  
pp. R7-R10 ◽  
Author(s):  
A P Silva ◽  
P Schoeffter ◽  
G Weckbecker ◽  
C Bruns ◽  
H A Schmid
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Corticotropin Releasing Hormone ◽  
Acth Secretion ◽  
Releasing Hormone ◽  
Corticosterone Secretion ◽  
Corticosterone Release ◽  
Acth Release

Objective: Adrenocorticotropic hormone (ACTH)-dependent Cushing’s syndrome is biochemically characterized by increased plasma concentrations of ACTH inducing hypersecretion of cortisol. Somatostatin is known to inhibit ACTH secretion, and in vitro data have shown the inhibition of ACTH secretion by agonists activating sst2 and sst5 receptors. The present study aimed to determine the inhibitory effect of the multireceptor ligand SOM230, compared with the sst2-preferring agonist octreotide, on corticotropin-releasing hormone (CRH)-stimulated secretion of ACTH and corticosterone in rats. Methods: Secretion of ACTH and corticosterone was induced by i.v. application of CRH (0.5 μg/kg) in rats pretreated 1 h before by i.v. application of SOM230 (1, 3, or 10 μg/kg), octreotide (10 μg/kg) or NaCl 0.9%. Results: SOM230 (3 and 10 μg/kg) inhibited CRH-induced ACTH release by 45±3% and 51±2%, respectively, and corticosterone release by 43±5% and 27±16%, respectively. 10 μg/kg of octreotide tended to be less potent at inhibiting ACTH release (34±6% inhibition) and did not alter the secretion of corticosterone. Conclusion: SOM230 has a stronger inhibitory effect on ACTH and corticosterone secretion than octreotide in rats. This difference can be explained by its higher affinity to sst1, sst3 and especially sst5 receptors compared with octreotide.

Effects of acute administration of 2-hydroxylated metabolites of oestrogens on LH and prolactin secretion in male and female prepubertal rats

1984 ◽  
Vol 103 (3) ◽  
pp. 317-325
Author(s):  
A. K. Brar ◽  
G. Fink
Keyword(s):  
Plasma Concentration ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Female Rat ◽  
Uterine Weight ◽  
Immature Female ◽  
Male And Female ◽  
Immature Male ◽  
Lh Release

ABSTRACT The effects of catechol oestradiol and catechol oestrone on the release of LH and prolactin were investigated in immature male and female Wistar rats. In male rats both catechol oestradiol and catechol oestrone significantly increased the plasma concentration of LH, and catechol oestradiol but not catechol oestrone significantly increased the plasma concentration of prolactin and decreased the pituitary concentration of LH. The parent oestrogens, oestradiol-17β and oestrone, had no effect on plasma LH concentrations, but both increased significantly the plasma concentration of prolactin, and oestrone but not oestradiol-17β increased the pituitary concentration of LH. In immature female rats, catechol oestradiol inhibited the surge of LH and the increase in uterine weight induced by injecting pregnant mare serum gonadotrophin (PMSG). The injection of oestrone induced an increase in the plasma concentration of LH which was about nine times greater than that produced by oestradiol-17β. There were no significant differences in the effects of these steroids on plasma prolactin concentration. These results (i) confirm that in the immature male rat catechol oestrogens can stimulate LH release and show that catechol oestradiol can increase prolactin release, (ii) show that catechol oestradiol can inhibit the stimulatory effects of PMSG on LH release and uterine weight in the immature female rat, and (iii) demonstrate that oestrone can stimulate LH release in the immature female rat. J. Endocr. (1984) 103, 317-325

Sign in / Sign up

Export Citation Format

Share Document