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.

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.

GONADOTROPHIN REGULATION IN THE LACTATING RAT

1978 ◽  
Vol 88 (3) ◽  
pp. 668-675 ◽  
Author(s):  
R. W. Steger ◽  
J. J. Peluso
Keyword(s):  
Positive Feedback ◽  
Post Partum ◽  
Ovariectomized Rats ◽  
Releasing Hormone ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Rh ◽  
Lh Releasing Hormone

ABSTRACT Post-partum lactation in the rat is associated with follicular quiescence and an attenuation of gonadotrophin secretion. The present study demonstrates that the lactating rat responds to exogenous LH-releasing hormone (LH-RH) in a manner similar to dioestrous rats. Oestrogen priming increases the LH and FSH response to LH-RH to a smaller degree in ovariectomized, lactating, than in non-lactating, ovariectomized rats. Pituitary LH levels throughout lactation did not seem to be related to LH-RH-induced LH release. A diminished post-castration rise in both LH and FSH, and a diminished positive feedback response to oestrogen administration were also observed and may indicate a disruption of gonadotrophin regulation at both the hypothalamic and the pituitary level.

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.

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

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.

DISSOCIATION IN THE REGULATION OF LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE IN A HYPERPROLACTINAEMIC RAT MODEL: INTERRELATIONSHIPS BETWEEN GONADOTROPHIN AND PROLACTIN CONTROL

1981 ◽  
Vol 90 (1) ◽  
pp. 41-51 ◽  
Author(s):  
J. A. F. TRESGUERRES ◽  
A. I. ESQUIFINO
Keyword(s):  
Positive Feedback ◽  
Follicle Stimulating Hormone ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Oestradiol Benzoate ◽  
Female Wistar Rats ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Releasing Hormone

Male and female Wistar rats were made hyperprolactinaemic by grafting two pituitary glands of litter-mate donors under the kidney capsule at 30 days of age. Other animals were sham-operated at the same age to serve as controls. Plasma levels of prolactin, LH and FSH were measured by double-antibody radioimmunoassay. Basal preoperative prolactin levels of ∼ 10 ng/ml increased after the transplantation in both male and female rats, reaching values of ∼ 180 ng/ml. Levels of LH were significantly reduced in these hyperprolactinaemic rats, whereas an increase in FSH values was seen. After administration of LH releasing hormone (LH-RH) a reduced LH response was seen but there was no response of FSH to LH-RH or even a decrease in FSH values. Prolactin levels were also reduced by LH-RH injection. Although an increase in prolactin levels was observed in control animals after a challenge with oestradiol benzoate, reduced increments were seen in experimental animals. The positive feedback effect of oestradiol benzoate on LH in females was reduced in pituitary-grafted rats but a potentiation of the FSH positive feedback could be clearly detected. This study suggests a dissociation of LH and FSH regulation in hyperprolactinaemia.

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.

EFFECT OF NOREPINEPHRINE SYNTHESIS INHIBITORS AND A DOPAMINE AGONIST ON HYPOTHALAMIC LH-RH, SERUM GONADOTROPHIN AND PROLACTIN LEVELS IN GONADAL STEROID TREATED RATS

1978 ◽  
Vol 89 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Satya P. Kalra ◽  
Pushpa S. Kalra ◽  
C. L. Chen ◽  
James A. Clemens
Keyword(s):  
Dopamine Agonist ◽  
Ovariectomized Rats ◽  
Prolactin Release ◽  
Feedback Effects ◽  
Medial Basal Hypothalamus ◽  
Serum Lh ◽  
Lh Release ◽  
Low Levels ◽  
Lh Rh ◽  
The Relationship

ABSTRACT The relationship between the medial basal hypothalamus (MBH) LH-RH activity and LH release was studied following progesterone (P) treatment of oestrogen-primed ovariectomized rats (day 0). Following P administration at 10.00 h (day 2) serum LH levels increased rapidly after 13.00 h to peak levels attained at 15.00 h and maintained until 18.00 h. Coincident with the onset of augmented release and peak serum LH concentrations at 15.00 h there was a significant enhancement in the MBH LH-RH activity. Thereafter, the MBH LH-RH stores promptly fell and remained at morning low levels through the rest of the LH surge period. P treatment also stimulated release of FSH and prolactin in the afternoon. Administration of norepinephrine (NE) synthesis inhibitors, diethyldithiocarbamate (DDC) and U-14,624 before P blocked the afternoon increments in serum gonadotrophins and the MBH LH-RH levels; prolactin release was also suppressed in DDC treated rats. In contrast, lergotrile mesylate (dopamine agonist) treatment prior to P administration suppressed only the afternoon increase in prolactin release. These studies show that (1) P can stimulate MBH LH-RH activity in oestrogen-primed rats and these effects are transmitted to the LH-RH peptidergic neurons via NE synapses in the preoptic area and (2) a common central NE system may mediate the stimulatory feedback effects of P on gonadotrophin and prolactin release.

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