Effect of sulpiride-induced hyperprolactinaemia on catecholamine turnover and LRH concentration in the medial basal hypothalamus of rats

1983 ◽  
Vol 102 (3) ◽  
pp. 321-326 ◽  
Author(s):  
Fumio Chatani ◽  
Toshihiro Aono ◽  
Koji Koike ◽  
Keiichi Tasaka ◽  
Keiichi Kurachi
Keyword(s):  
High Performance Liquid Chromatography ◽  
High Performance ◽  
Serum Levels ◽  
Female Rats ◽  
Monoamine Oxidase Inhibition ◽  
Medial Basal Hypothalamus ◽  
Catecholamine Turnover ◽  
Serum Lh ◽  
Oxidase Inhibition ◽  
Lh Secretion

Abstract. In order to clarify the mechanism of hyperprolactinaemic anovulation, the medial basal hypothalamic (MBH) catecholamine (CA) turnover and LRH concentration, and the serum levels and pituitary contents of gonadotrophins and prolactin (Prl) in hyperprolactinaemic female rats were examined. Hyperprolactinaemia (HPrl) was produced by oral administration of sulpiride for 10 consecutive days; each measurement made on the sulpiride-treated rats was compared with that of control dioestrus rats. Prl, LH, FSH and LRH were determined by radioimmunoassay; CA turnover, as assessed by the accumulation of CA following monoamine oxidase inhibition, was assayed by high performance liquid chromatography with electrochemical detection. Sulpiride treatment induced (1) an increase in the serum Prl and a decrease in the serum LH, (2) an increase in the pituitary FSH and LH contents, (3) an increase in the MBH LRH concentration, and (4) an increase in the MBH dopamine (DA) turnover. These results suggest that HPrl may induce anovulation by impaired LH secretion which was caused by the suppression of LRH release due to an increase in DA turnover in the MBH.

Influence of anti-oestrogens on gonadotrophin secretion in control and ACTH-infused immature rats

1984 ◽  
Vol 105 (3) ◽  
pp. 308-313 ◽  
Author(s):  
David R. Mann ◽  
Michael S. Blank ◽  
R. Sridaran ◽  
V. Daniel Castracane ◽  
Charles Eldridge ◽  
...  
Keyword(s):  
Serum Testosterone ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Constant Infusion ◽  
Simultaneous Treatment ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Immature Rats ◽  
Lh Secretion

Abstract. The objective of this study was to determine whether anti-oestrogens (nafoxidine, MER-25) would block the suppressive effects of ACTH on gonadotrophin secretion in immature rats. Female rats were castrated at 25–26 days of age, and an Alzet osmotic minipump containing ACTH (1–24) or saline was implanted in each animal. ACTH was administered at a rate of 1 IU/day by constant infusion. Beginning on the day of surgery, animals were injected daily for 5 days with 0.25, 5 or 25 μg/100 g body weight of nafoxidine or 5 mg MER-25 and sacrificed on the sixth day following castration. ACTH lowered serum LH concentrations and increased pituitary LH levels. Serum androstenedione concentrations were more than two times greater in ACTH-infused than in control rats, but serum oestrone levels were not affected. Serum testosterone and oestradiol concentrations in ACTH-infused rats remained below levels of detection. Administration of 0.25 μg of nafoxidine prevented the suppressive effects of ACTH on serum LH. Serum levels of LH in these animals were comparable to saline-treated controls (418 ± 94 vs 443 ± 73 ng/ml). The two higher doses of nafoxidine and MER-25 were ineffective in suppressing the actions of ACTH on serum LH. MER-25 reduced serum LH values in both controls and ACTH-infused rats. Serum FSH concentrations were not altered by ACTH or nafoxidine treatment. MER-25 elevated pituitary FSH concentrations in both control and ACTH-infused rats. These data suggest that the inhibitory effect of ACTH on LH secretion in immature rats is mediated by an oestrogenic steroid, since this action can be blocked by simultaneous treatment with a low dose of the anti-oestrogen, nafoxidine.

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
Keyword(s):  
Binding Sites ◽  
Limit Of Detection ◽  
Serum Levels ◽  
Female Rats ◽  
Serum Prolactin ◽  
Hormonal Changes ◽  
Subsequent Increase ◽  
Serum Progesterone ◽  
Serum Lh ◽  
Prostaglandin F

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.

EFFECT OF SYNTHETIC THYROTROPHIN RELEASING FACTOR ON PROLACTIN AND LUTEINIZING HORMONE SECRETION IN MALE AND FEMALE RATS DURING VARIOUS REPRODUCTIVE STATES

1975 ◽  
Vol 67 (3) ◽  
pp. 425-430 ◽  
Author(s):  
R. P. DEIS ◽  
NIA ALONSO
Keyword(s):  
Hormone Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Serum Prolactin ◽  
Serum Prolactin Level ◽  
Luteinizing Hormone Secretion ◽  
Male And Female Rats ◽  
Serum Lh ◽  
The Mean ◽  
Lh Secretion

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.

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.

scholarly journals Erythropoietin-producing hepatocellular receptor A7 restrains estrogen negative feedback of luteinizing hormone via ephrin A5 in the hypothalamus of female rats

2020 ◽  
Vol 319 (1) ◽  
pp. E81-E90 ◽  
Author(s):  
Shang Li ◽  
Junyu Zhai ◽  
Bing Xu ◽  
Jiansheng Liu ◽  
Weiwei Chu ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Female Rats ◽  
Female Rat ◽  
Female Reproduction ◽  
Systemic Injection ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
17Β Estradiol ◽  
Lh Secretion

We have previously shown that systemic injection of erythropoietin-producing hepatocellular receptor A7 (EPHA7)-Fc raises serum luteinizing hormone (LH) levels before ovulation in female rats, indicating the induction of EPHA7 in ovulation. In this study, we aimed to identify the mechanism and hypothalamus-pituitary-ovary (HPO) axis level underlying the promotion of LH secretion by EPHA7. Using an ovariectomized (OVX) rat model, in conjunction with low-dose 17β-estradiol (E2) treatment, we investigated the association between EPHA7-ephrin (EFN)A5 signaling and E2 negative feedback. Various rat models (OVX, E2-treated OVX, and abarelix treated) were injected with the recombinant EPHA7-Fc protein through the caudal vein to investigate the molecular mechanism underlying the promotion of LH secretion by EPHA7. Efna5 was observed strongly expressed in the arcuate nucleus of the female rat by using RNAscope in situ hybridization. Our results indicated that E2, combined with estrogen receptor (ER)α, but not ERβ, inhibited Efna5 and gonadotropin-releasing hormone 1 ( Gnrh1) expressions in the hypothalamus. In addition, the systemic administration of EPHA7-Fc restrained the inhibition of Efna5 and Gnrh1 by E2, resulting in increased Efna5 and Gnrh1 expressions in the hypothalamus as well as increased serum LH levels. Collectively, our findings demonstrated the involvement of EPHA7-EFNA5 signaling in the regulation of LH and the E2 negative feedback pathway in the hypothalamus, highlighting the functional role of EPHA7 in female reproduction.

Postovulatory steroidogenesis after PMS-induced ovulation in immature female rats

1981 ◽  
Vol 241 (3) ◽  
pp. E221-E225 ◽  
Author(s):  
K. Taya ◽  
G. S. Greenwald
Keyword(s):  
Serum Levels ◽  
Female Rats ◽  
Corpora Lutea ◽  
Adult Rats ◽  
Rat Serum ◽  
Follicular Maturation ◽  
Adult Rat ◽  
Serum Lh

Thirty-day-old rats given a single subcutaneous injection of 5 IU pregnant mare serum gonadotropin (PMS) at 0900 h ovulated on the morning of day 33 (= estrus). However, the second ovulation did not occur until 9.4 days later. To determine the mechanism responsible for the delay in the second ovulation, in vivo and in vitro determinations of steroid and peptide hormones were compared between PMS-primed immature rats and adult cyclic rats. In PMS-primed rats, the corpora lutea (CL) produced progesterone for 2 days longer (until day 36) than the CL of the adult rat. Serum levels of 20 alpha-dihydroprogesterone, testosterone, and estradiol in PMS-primed rats were significantly lower than the corresponding values in adult rats. Serum LH was consistently lower in the PMS-primed rats. An increase in serum FSH occurred on days 36–37, which may be responsible for maturation of the follicles destined to ovulate at the second ovulation. On day 37, the nonluteal ovary of the PMS-primed rats also began to produce in vitro appreciable amounts of testosterone and estradiol. These findings suggest that the greater levels of prolactin and/or low levels of luteinizing hormone during estrus in PMS-primed rats may be responsible for the prolonged secretion of progesterone by the CL. This in turn inhibits follicular maturation, indirectly by lowering serum LH, which is reflected in reduced ability of the follicles in vitro to produce testosterone and estradiol until the CL regress.

The synthesis and release of gonadotropins in response to gonadotropin-releasing hormone of the rat anterior pituitary gland during weight reduction

1990 ◽  
Vol 122 (5) ◽  
pp. 628-632 ◽  
Author(s):  
Fumikazu Kotsuji ◽  
Takeshi Aso ◽  
Naoyuki Kamitani ◽  
Toshiro Tominaga
Keyword(s):  
Weight Loss ◽  
Pituitary Gland ◽  
Weight Reduction ◽  
Female Rats ◽  
Serum Lh ◽  
Female Wistar Rats ◽  
Progressive Weight Loss ◽  
Lh Release ◽  
Lh Secretion

Abstract. It is well recognized that weight reduction produces the suppression of serum LH but not FSH level in rodents. In order to clarify the mechanism by which the discrepancy between LH and FSH levels is brought about, the influence of weight loss on the pituitary function was explored using female rats. The changes of the pituitary response to GnRH and the basal secretion of gonadotropins with progressive weight loss were investigated by in vitro short-term incubation of the pituitary gland after prolonged weight loss in female Wistar rats. On the first day of diestrous and until day 14 of the diet, GnRH induced LH and FSH release from the pituitary and a decrease in pituitary content of them, but the total amount of gonadotropin in culture medium and pituitary tissue was not affected. On day 30 of the diet, the decrease in pituitary content disappeared. On day 60 LH release disappeared, whereas pituitary FSH and the total amount of gonadotropins were increased by GnRH. Non-stimulated FSH but not LH secretion per mg of pituitary was augmented during dieting. The data indicate that pituitary responsiveness to GnRH and non-stimulated FSH release were modified by weight loss: the LH-releasing action of GmRH was diminished, the gonadotropin-synthesizing action of GnRH was augmented, and non-stimulated FSH release was increased.

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