THE INFLUENCE OF TIME, DOSE AND GONADAL STEROIDS ON LH-RH-INDUCED GONADOTROPHIN RELEASE IN RATS

1975 ◽  
Vol 78 (4) ◽  
pp. 695-704 ◽  
Author(s):  
Wolfgang Lotz
Keyword(s):  
Time Course ◽  
Time Lapse ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Response Curves ◽  
Intact Male ◽  
Maximal Increase ◽  
Serum Lh ◽  
Lh Rh ◽  
Lh Releasing Hormone

ABSTRACT Hypophyseal responses to LH-releasing hormone (LH-RH) were studied in ovariectomized rats, pre-treated once with 50 μg oestradiol-3-benzoate alone or in combination with 25 mg progesterone either 16, 24, 48 or 72 h before the administration of LH-RH. The highest serum gonadotrophin increase was detected in ovariectomized rats pre-treated with oestrogen 48 h before the LH-RH injection. The serum LH concentration change in intact male rats was markedly lower in terms of order of magnitude than in ovariectomized, oestradiol-3-benzoate, progesterone-treated rats ("O. Oe. P."-rats). These latter test animals showed the maximal increase of serum LH concentration, depending on the dose of LH-RH, after 10 to 25 min and that of FSH after 40 min. The dose-response curves for LH release in "O. Oe. P."-rats were linear for short (10 and 15 min) and sigmoid for longer time intervals (20, 30 and 40 min) between LH-RH injection and sacrifice. The possible reasons for the difference in both magnitude and time-lapse for maximal increase of serum LH and FSH concentration, the influence of steroid pre-treatment and the variation of the time-course of serum LH concentration, depending on the dose of LH-RH, are discussed.

Serotonin-reinstatement of luteinizing hormone surges after loss of positive feedback in ovariectomized rats bearing subcutaneous capsules containing oestrogen

1983 ◽  
Vol 98 (1) ◽  
pp. 7-17 ◽  
Author(s):  
R. F. Walker
Keyword(s):  
Positive Feedback ◽  
Ovariectomized Rats ◽  
Facilitatory Effect ◽  
Serum Progesterone ◽  
Serotonin Content ◽  
Serum Lh ◽  
Serotonin Turnover ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Feedback Responses

In ovariectomized rats treated chronically with oestrogen there is a loss of positive feedback effects on LH secretion. This was not due to depletion of pituitary LH since injection of LH releasing hormone (LH-RH; 50 ng/100 g body wt) caused a significant (P < 0·01) rise in serum LH even after the loss of spontaneous LH surges. However, the magnitude of the increase in serum LH in response to LH-RH was greater (412 ± 41 μg/l) before than after (291 ± 29 μg/l) loss of the LH surges. Excessive blood sampling was also not responsible, since positive feedback responses declined comparably in rats bled daily or once every 3–4 days. Progesterone (0·5 mg s.c.), administered for 5 consecutive days, failed to restore LH surges indicating that deficiency of this steroid after ovariectomy does not cause positive feedback responses to disappear in rats exposed chronically to oestrogen. Moreover regular daily fluctuations in serum progesterone, probably of adrenal origin, occurred before as well as after daily LH surges were lost. Serotonin content and turnover were depressed (P < 0·05) when ovariectomized rats first received the subcutaneous capsules containing oestrogen. This change correlated temporally with the onset of daily LH surges and was eventually lost. After 30 days exposure to oestrogen, serotonin turnover increased (P < 0·01) and positive feedback responses were absent. Catecholamine levels and turnover did not show differential responses to oestrogen and were depressed after acute as well as chronic steroid treatment. p-Chlorophenylalanine (pCPA; 250 mg/kg)+ l-dihydroxyphenylalanine (l-DOPA; 200 mg/kg), which depress serotonin and enhance catecholamine synthesis respectively, failed to reinstate LH surges, but these were restored in 22% of the rats receiving l-DOPA alone. pCPA, followed 2 days later by 5-hydroxytryptophan (5-HTP) at 11.00 h, reinstated LH surges in 88% of rats, and a dose–response curve showed that as little as 4 mg 5-HTP/kg stimulated repetitive LH surges when given with pCPA according to this schedule. However, the administration of α-methyl-p-tyrosine + l-DOPA, an analogous treatment involving catecholamines, was only marginally effective (15%). These findings suggest that perturbations of monoamine metabolism occurring in ovariectomized rats exposed to oestrogen for several weeks contribute to loss of daily LH surges. Since pCPA + 5-HTP restored LH surges most effectively, then positive feedback may disappear as the facilitatory effect of serotonin is lost after chronic oestrogen administration.

EflFect of Testosterone and Estradiol on the LH and FSH Release Induced by LH-Releasing Hormone (LH-RH) in Intact Male Rats*

Endocrinology ◽  
1972 ◽  
Vol 90 (6) ◽  
pp. 1578-1581 ◽  
Author(s):  
LUCIANO DEBELJUK ◽  
AKIRA ARIMURA ◽  
ANDREW V. SCHALLY
Keyword(s):  
Male Rats ◽  
Intact Male ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Releasing Hormone

FEEDBACK EFFECT OF OESTROGEN ON LUTEINIZING HORMONE SECRETION BY THE RAT PITUITARY GLAND

1982 ◽  
Vol 92 (3) ◽  
pp. 389-395 ◽  
Author(s):  
TAKASHI HIGUCHI ◽  
MASAZUMI KAWAKAMI
Keyword(s):  
Pituitary Gland ◽  
Hormone Secretion ◽  
Feedback Effect ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Secretion ◽  
Hypothalamic Area ◽  
Serum Lh ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Lh Secretion

Ovariectomized rats with neural deafferentation at the level of the posterior border of the anterior hypothalamic area (AC rats) were used to re-evaluate the direct feedback effect of oestrogen on the regulation of LH secretion by the pituitary gland. Synthetic LH releasing hormone (LH-RH; 300 ng/kg), injected at 30-min intervals into AC rats with undetectable basal LH, induced pulsatile increase of serum LH concentrations. Oestradiol-17β (5 μg), administered i.v. just before the first LH-RH injection, significantly decreased the LH response to a second injection of LH-RH given 30 min later and to subsequent injections. Maximal inhibition was 58%. Oestradiol-17β (5 μg) given i.v. to control ovariectomized rats decreased serum LH concentrations 40 min after administration; the maximum reduction being 52%. An s.c. injection of oestradiol benzoate (5 μg) increased pituitary responsiveness to LH-RH by the next day in AC rats but decreased serum LH levels in control ovariectomized rats. These results indicate that acute inhibitory and chronic facilitatory effects of oestrogen on LH secretion are exerted at the pituitary gland, without a change in LH-RH secretion. The prolonged inhibitory effect of oestrogen is at the level of the hypothalamus and causes a reduction in LH-RH secretion.

RESTORATION OF OESTROGEN POSITIVE FEEDBACK EFFECT ON LH RELEASE BY BROMOCRIPTINE IN HYPERPROLACTINAEMIC PATIENTS WITH GALACTORRHOEA-AMENORRHOEA

1979 ◽  
Vol 91 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takenori Shioji Motoi Yasuda ◽  
Koji Koike ◽  
Keiichi Kurachi
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Prolactin ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
The Mean ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Positive Feedback Effect

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.

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

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.

EFFECTS OF NALOXONE ON LUTEINIZING HORMONE AND PROLACTIN IN SERUM OF RATS

1980 ◽  
Vol 85 (2) ◽  
pp. 307-315 ◽  
Author(s):  
M. S. BLANK ◽  
A. E. PANERAI ◽  
H. G. FRIESEN
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Immature Female ◽  
Subcutaneous Injections ◽  
Serum Lh ◽  
Opiate Peptides ◽  
Lh Release ◽  
Lh Secretion

The effects of subcutaneous injections of the opiate antagonist naloxone on the tonic and phasic secretion of prolactin and LH were studied in rats. During development, resting levels of prolactin in serum were decreased by naloxone (2·5 mg/kg body wt) on days 24,45 and 50 in female rats and on days 28,45 and 50 in male rats. In the adult, naloxone (2·5 mg/kg body wt) decreased basal levels of serum prolactin in male rats and levels during oestrus in female rats. In 25-day-old female rats, serum LH rose from resting levels within 7·5 min of naloxone administration (2·5 mg/kg body wt) and returned to pretreatment levels by 30 min, while prolactin fell by 7·5 min and remained low for as long as 60 min after treatment. Furthermore, a tenfold lower dose of naloxone (0·25 mg/kg body wt) did not raise basal levels of serum LH but still decreased resting levels of serum prolactin in immature female rats (24 days old). The effect of naloxone (2·5 mg/kg body wt) on phasic LH release was studied in 29-day-old immature female rats primed on day 27 with pregnant mare serum gonadotrophin (PMSG). In these PMSG-treated rats the onset of the prolactin surge was blunted by naloxone while it had no effect on phasic LH release. Naloxone (5 mg/kg body wt) also induced a rise in levels of serum LH in ovariectomized rats and, if administered with morphine, it reversed the short-term inhibition of LH secretion caused by morphine. However, naloxone was ineffective after pretreatment with oestradiol benzoate. These findings suggest that the responses of serum LH and prolactin to naloxone were dissociated and that oestrogens and opiate peptides may have interacted to regulate secretion of LH.

CIRCADIAN RHYTHM OF LUTEINIZING HORMONE SECRETION IN THE OVARIECTOMIZED RAT IMPLANTED WITH OESTRADIOL

1977 ◽  
Vol 75 (2) ◽  
pp. 251-260 ◽  
Author(s):  
G. CHAZAL ◽  
M. FAUDON ◽  
F. GOGAN ◽  
M. HERY ◽  
C. KORDON ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Secretion ◽  
Implantation Time ◽  
Light Darkness ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Afternoon Peak

Implantation of a solid source of oestradiol into ovariectomized rats produced constant plasma concentrations of the hormone over a long period of time. Under these conditions, LH is released in a circadian pattern with a very marked peak in the afternoon. This circadian rhythm is synchronized to the light–darkness cycle, since it follows exactly a shift in the nycthemeral cycle. The first peak appeared on day 3 after placement of the oestrogen implant; its amplitude was constant from days 3 to 9 after implantation, and decreased gradually during prolonged implantation. The afternoon peak was not correlated with changes in the pituitary sensitivity to exogenous LH releasing hormone (LH-RH), since the LH response to increasing doses of the peptide could be superimposed in the morning and in the afternoon. However, the decreased amplitude of the rhythm observed after more than 9 days of implantation seemed to depend upon a progressive desensitization of the pituitary gland to LH-RH. Pituitary LH content also decreased as a function of implantation time. It is concluded that, under conditions of constant plasma oestradiol concentrations and of constant pituitary sensitivity to LH-RH, a daily activation of the neural trigger releasing pituitary gonadotrophins occurs.

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