THE SEQUENCE OF HORMONAL CHANGES DURING PROSTAGLANDIN INDUCED LUTEOLYSIS OF THE SUPERLUTEINIZED RAT OVARY

1978 ◽  
Vol 87 (3) ◽  
pp. 617-624 ◽  
Author(s):  
P. A. Torjesen ◽  
R. Dahlin ◽  
E. Haug ◽  
A. Aakvaag

ABSTRACT Immature female rats were pre-treated with pregnant mare's serum gonadotrophin (PMSG) and human chorionic gonadotrophin (HCG) to achieve superluteinization. Eight days after the HCG administration luteolysis was induced by sc injection of 5 μg of the prostaglandin F2α (PGF2α) analogue cloprostenol (Estrumate®). The serum levels of progesterone, 20α-dihydroprogesterone (20α-DHP), prolactin (PRL) and luteinizing hormone (LH) as well as the number of ovarian LH binding sites were measured during the first 23 h after cloprostenol injection. The serum levels of progesterone decreased from 500 to 200 ng/ml within 25 min after cloprostenol administration. A further decrease to 20 ng/ml occurred during the next 4 h, and serum progesterone remained low for the rest of the period. An increase in serum prolactin (PRL) to values between 28 and 44 ng/ml was observed after 3 h and the values remained elevated for the next 7 h. Although the serum levels of progesterone declined immediately, the serum 20α-dihydroprogesterone (20α-DHP) levels remained at 60 to 140 ng/ml for the first 5 h and then gradually increased to values corresponding to the initial progesterone levels 14 to 23 h after treatment. The number of ovarian LH binding sites was between 1.2 and 1.4 × 10−12 mol/mg protein during the first 9 h after prostaglandin (PG) injection, and then decrreased to 0.8 and 0.5 × 10−12 mol/mg protein at 14 and 23 h, respectively. The serum LH levels remained below the limit of detection for the assay (10 ng/ml) throughout the observation period. PGF2α injection induced the same basic changes in the serum levels of progesterone and 20α-DHP as cloprostenol treatment. Thus, the first effect of PG treatment measured was an immediate decline in the serum levels of progesterone, and this decline probably initiated the subsequent increase in pituitay PRL and ovarian 20α-DHP secretion. Therefore, the decrease in the number of ovarian LH binding sites appeared to be a consequence rather than a mediator of luteolytic effects of the prostaglandins.

1978 ◽  
Vol 87 (3) ◽  
pp. 625-631 ◽  
Author(s):  
P. A. Torjesen ◽  
R. Dahlin ◽  
E. Haug ◽  
A. Aakvaag

ABSTRACT Twenty-five day old female rats were treated with pregnant mare's serum gonadotrophin (PMSG) and human chorionic gonadotrophin (HCG) to achieve a state of luteinization. Eight days after the HCG administration luteolysis was induced by a subcutaneous injection of 5 μg of the prostaglandin F2α analogue cloprostenol (Estrumate®, ICI 80996). In animals treated with 2-Br-α-ergocryptine (BEC), administration of cloprostenol decreased serum progesterone levels from 580 to 20 ng/ml in 5 h and progesterone remained low for the next 18 h. The serum levels of 20α-dihydroprogesterone (20α-DHP) and prolactin (PRL) remained at pre-treatment values (20α-DHP 85 to 170 ng/ml; PRL less than 5 ng/ml) throughout the observation period. When animals treated with both BEC and cloprostenol were given PRL 5 h after the prostaglandin injection, an increased 20α-DHP level (630 ng/ml) was found 23 h after the cloprostenol administration, while the progesterone level was decreased (70 ng/ml). These findings were similar to the observations following cloprostenol treatment alone. The study indicates a causal relationship between the increase in the serum levels of PRL and 20α-DHP observed after PGF2α induced luteolysis in rats with superluteinized ovaries.


1986 ◽  
Vol 110 (3) ◽  
pp. 423-428 ◽  
Author(s):  
G. A. Jahn ◽  
R. P. Deis

ABSTRACT Ether stress applied at 10.00 h induced a 100% increase in serum prolactin in intact and ovariectomized androgenized rats. Ovariectomy significantly diminished the basal serum prolactin values observed in intact androgenized rats. Two doses of progesterone (5 mg) given to intact and ovariectomized androgenized rats 14 and 2 h before exposure to ether stress increased prolactin values in the control groups but completely prevented the effect of stress. Exposure to ether stress induced a 100% increase in serum prolactin values in androgenized rats with increased serum progesterone levels 4 days after the induction of ovulation and the luteal phase with human chorionic gonadotropin (hCG). A group of androgenized rats with induced maternal behaviour and which had been suckled for 6 days was given 100 i.u. hCG and suckled for another 6 days after the hCG-induced luteal phase had been established. The serum prolactin and progesterone values of these rats were significantly higher than those treated with hCG only and ether stress did not increase prolactin release. A greatly increased serum concentration of prolactin was obtained in pro-oestrous and oestrous virgin rats after exposure to ether stress. Serum prolactin was also increased by stress in male rats. Progesterone administration to these female and male rats prevented stress-induced prolactin release. To ascertain the part played by dopamine and serotonin in the effect of stress on prolactin release, groups of androgenized and oestrous female rats were treated with bromocriptine or p-chlorophenylalanine methylester hydrochloride (pCPA). The dopaminergic agonist bromocriptine markedly reduced prolactin levels in the unstressed androgenized rats, but did not prevent the prolactin increases induced by stress. Administration of pCPA had no effect on basal or stress-increased serum levels of prolactin. It is concluded that modifications of the ovarian steroid secretions, especially of progesterone, has profound effects on prolactin release in response to ether stress. The release of the hormone was not mediated by a dopaminergic or serotonergic regulatory pathway. J. Endocr. (1986) 110, 423–428


1982 ◽  
Vol 100 (4) ◽  
pp. 481-485 ◽  
Author(s):  
F. R. Pérez-López ◽  
C. M. González-Moreno ◽  
M. D. Abós ◽  
J. A. Andonegui ◽  
R. H. Corvo

Abstract. In order to determine whether or not pituitary responsiveness to the dopaminergic antagonist clebopride changes during the nyctohemeral cycle, 10 healthy women with regular cycles were given 1 mg of clebopride orally at 09.00 h and 24.00 h with at least a 5 day interval between each test. In addition, 5 of the women were given a placebo instead of clebopride at midnight to evaluate the spontaneous hormonal changes. During the 24.00 h test the women had significantly higher P < 0.05) mean TSH basal levels. Serum prolactin (Prl) increased significantly (P < 0.001) after clebopride administration while these changes did not occur when placebo was used instead of clebopride at midnight. The Prl response to clebopride was qualitatively similar at 09.00 h and at 24.00 h. Clebopride given at midnight induced a significant increase (P < 0.05) in serum TSH while this change did not occur when the drug was given at 09.00 h or when placebo was given at midnight. The administration of clebopride resulted in no discernible alterations in serum LH, FSH or GH in either the 09.00 h or the 24.00 h tests. Thus, Prl responses to clebopride were similar in the morning and at midnight, TSH significantly increased after clebopride at midnight whereas this did not occur when the drug was given in the morning, and no significant changes were induced in LH, FSH or GH at the times studied.


1992 ◽  
Vol 263 (3) ◽  
pp. E507-E511 ◽  
Author(s):  
D. Dondi ◽  
P. Limonta ◽  
R. Maggi ◽  
F. Piva

These experiments were performed to analyze whether treatments of ovariectomized female rats with ovarian steroid regimens able to induce either an increase (positive feedback effect) or a decrease (negative feedback effect) of serum levels of luteinizing hormone (LH) have some impact on the characteristics of mu-opioid binding sites in circumscribed areas of the brain. The increase of serum levels of LH elicited by a treatment with estradiol benzoate (EB) plus progesterone (P; positive feedback effect) was accompanied by a significant decrease in the number of mu-binding sites in the hypothalamus and in the corpus striatum. The decrease in serum levels of LH induced by a treatment with EB alone (negative feedback effect) brought about a significant increase of the number of mu-binding sites in the thalamus and in the hippocampus. These results seem to suggest that the release of LH induced by EB plus P may involve a decrease of hypothalamic mu-binding sites. Apparently, the inhibitory effect on LH release exerted by EB alone does not involve any change of the density of these binding sites in the hypothalamus.


1979 ◽  
Vol 83 (2) ◽  
pp. 131-139 ◽  
Author(s):  
W. BECK ◽  
W. WUTTKE

Six male rhesus monkeys were kept under rigidly controlled conditions for 1–2 years. During August of the first year a thyrotrophin releasing hormone (TRH) test was performed on each of the monkeys by giving 10 μg TRH as a bolus injection. Significantly increased serum prolactin levels occurred 15 min after the injection. After a training period of 2 months, during which blood samples were collected every other day by puncture of the saphenous vein, blood was collected three times a week for 14 months. Serum levels of prolactin, LH, FSH and testosterone were measured by radioimmunoassay. Mean serum prolactin levels increased significantly during June, July and August in all six animals. Peak levels were observed in August and September and then levels declined gradually to reach a minimum in April and May. Mean serum testosterone levels closely paralleled the annual pattern of prolactin. Mean serum LH levels significantly decreased during the time when mean serum prolactin and testosterone levels were increasing and they increased again at the time of decreasing mean prolactin levels, i.e. mean serum LH and prolactin were negatively correlated. In individual monkeys, however, a rigid negative correlation between serum prolactin and LH could not be demonstrated. Mean serum FSH levels did not change significantly.


1975 ◽  
Vol 67 (3) ◽  
pp. 425-430 ◽  
Author(s):  
R. P. DEIS ◽  
NIA ALONSO

SUMMARY The effect of synthetic thyrotrophin releasing factor (TRF) on serum prolactin and LH concentrations was determined by radioimmunoassay in male, cyclic and pseudopregnant female rats. A solution of TRF (0·1, 0·25, 0·5 and 1 μg/rat) was injected i.v. at 17.00 h into rats pretreated with sodium pentobarbitone at 13.00 h. A group of male rats was also treated with TRF at 11.00 h after pretreatment with sodium pentobarbitone at 07.00 h. Fifteen minutes after TRF administration, blood samples were obtained by heart puncture. Doses of 0·25, 0·5 and 1 μg TRF significantly increased the serum prolactin concentration in pro-oestrous rats. The mean serum prolactin level after the injection of 0·5 and 1 μg into oestrous rats and 0·5 μg TRF into dioestrous day 2 rats, was significantly greater than the control values. Injection of TRF on day 1 of dioestrus had no effect. Serum LH concentration was not significantly modified by the various doses of TRF administered. On day 3 of pseudopregnancy a significant increase of serum prolactin values was obtained with 0·5 and 1 μg TRF. On day 7 of pseudopregnancy a dose of 0·5 μg produced the same effect, but on day 10 of pseudopregnancy only 1 μg TRF significantly increased serum prolactin levels when compared with the control rats. In male rats serum prolactin concentration was significantly greater than the control values after TRF treatment either in the morning or the afternoon. The response was similar to that obtained in pro-oestrous rats. The results suggest that the ability of synthetic TRF to stimulate prolactin release exists in both female and male rats and that TRF does not affect LH secretion.


1977 ◽  
Vol 86 (3) ◽  
pp. 489-497 ◽  
Author(s):  
K.-D. Döhler ◽  
K. Gärtner ◽  
A. von zur Mühlen ◽  
U. Döhler

ABSTRACT Groups of adult male rats were decapitated without anaesthesia 30 seconds or 5, 10, 15 and 60 min after disturbance stress (investigators entering the animal room and moving the cages). The serum concentrations of LH, FSH, TSH, prolactin, triiodothyronine (T3) and thyroxine (T4) were measured by radioimmunoassay and corticosterone by a fluorometric method. With regard to the hormone levels measured in serum obtained within 30 seconds after induction of disturbance stress to resemble most closely the actual unstressed levels of endogenous hormones in circulation, serum corticosterone levels increased within 5 min. indicating that the procedure was stressful to the animals. In addition the serum prolactin and TSH levels were significantly elevated within 5 min, T3 within 60 min. Whereas corticosterone reached peak levels after 15 min. the serum levels of prolactin, TSH and T3 were still rising after 60 min. The FSH levels remained rather stable during the first 10 min. but started to rise during the following 5 min. At 60 min FSH levels were back to normal. Serum LH and T4 showed only minor fluctuations during the experimental period. These results indicate, that not only is the pituitary-adrenal axis stimulated by emotional stress, but also the pituitary-thyroid axis. It also seems, that emotional stress leads to a general activation of pituitary hormone release. Hence, proper care should be taken with regard to animal keeping, handling and the method of blood collection when dealing with rats as experimental animals.


1976 ◽  
Vol 83 (2) ◽  
pp. 269-279 ◽  
Author(s):  
K. D. Döhler ◽  
W. Wuttke

ABSTRACT Diurnal variations in serum hormone levels during 2 different stages of prepubertal development were investigated in male and female rats. Groups of 13 to 18 and 25 to 30 day old male and female rats were decapitated at 4-hour by intervals during a period of 24 h. Their blood was collected and hormones were measured by radio-immunoassay. FSH levels were constantly high in 13 to 18, but low in 25 to 30 day old females. FSH was low in younger males, and significantly higher but without diurnal fluctuations in the older males. Serum LH was low in approximately 40% of the 13 to 18 day old females, while 40% had moderately high levels, and the remaining females extremely high levels of the hormone. Most of the extremely high LH peaks were found at 15.00 h and some at 03.00 h. Older females and males of both age groups had constantly low serum LH levels. Serum oestradiol was high in males and females during days 13 to 18, but it was lower in the 25 to 30 day old animals. In the young females prolactin was slightly elevated between 15.00 h and 19.00 h, while in the males the serum prolactin fluctuations were not significant. Serum testosterone was low in females at all times. The 13 to 18 day old males had higher testosterone levels than the 25 to 30 day old males. Both groups showed slight, but insignificant fluctuations in serum testosterone. These results confirm result published previously and furthermore they demonstrate the existence of circasemedian or circadian rhythms for both the gonadotrophins and gonadal steroids. These results, also suggest that the maturation of the positive feedback action of oestradiol on gonadotrophin release in female rats occurs between day 10 and 20.


1980 ◽  
Vol 85 (2) ◽  
pp. 307-315 ◽  
Author(s):  
M. S. BLANK ◽  
A. E. PANERAI ◽  
H. G. FRIESEN

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.


1977 ◽  
Vol 86 (1) ◽  
pp. 162-172 ◽  
Author(s):  
Peter A. Torjesen ◽  
Asbjørn Aakvaag

ABSTRACT The process of luteolysis has been studied in immature rats in which superluteinization had been induced with pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotrophin (HCG). Following prostaglandin F2α and the prostaglandin analogues, and at the end of the pseudopregnancy, the plasma levels of progesterone and 20α-dihydroprogesterone were measured and used as parameters of luteal function in relation to the capacity of the ovarian tissue to bind LH, FSH and prolactin (PRL) in vitro. On day 19 after HCG a marked decrease in the progesterone level from the day 8 level was observed concomitant with a marked increase in 20α-dihydroprogesterone. The capacity of the ovarian tissue to bind LH in vitro was markedly reduced on day 19 compared to day 8. Identical changes were observed 21 h after 1 mg prostaglandin F2α or prostaglandin analogues. Progesterone decreased from about 600 ng/ml to about 50 ng/ml, whereas the increase in 20α-dihydroprogesterone was from about 200 ng/ml to 500–1000 ng/ml and the reduction in LH binding sites was from 1.7 × 10−12 to 0.5 × 10−12 mol/mg protein. Nanogram amounts of the analogues were as effective as 1 mg of prostaglandin F2α. The number of FSH or PRL binding sites was not affected by spontaneous luteolysis or the treatment given. By the use of graded doses of the prostaglandin analogues a negative correlation (r=−0.81) was found between plasma progesterone and 20α-dihydroprogesterone levels, and a positive correlation (r = 0.84) between LH binding sites and plasma progesterone levels. The luteolysis induced by prostaglandin F2α or prostaglandin analogues was indistinguishable from the spontaneous luteolysis using these parameters.


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