Anaesthesia with alphaxalone plus alphadolone acetate blocks the oestrogen-stimulated LH surge and impairs pulsatile LH secretion in ovariectomized female rats

1984 ◽  
Vol 102 (1) ◽  
pp. 27-31 ◽  
Author(s):  
R. G. Dyer ◽  
S. Mansfield
Keyword(s):  
Body Weight ◽  
Female Rats ◽  
Lh Surge ◽  
Group Of Seven ◽  
Oestradiol Benzoate ◽  
Anaesthetized Rats ◽  
Lh Secretion

ABSTRACT Two experiments were undertaken to assess further the action of the steroid anaesthetic alphaxalone upon LH secretion in chronically ovariectomized female rats. For the first experiment, 31 rats were given two injections of oestradiol benzoate (20 μg/100 g body weight), each 72 h apart, to stimulate an LH surge 6 h after the second injection. However, one group of seven rats was anaesthetized with alphaxalone throughout the 6-h period and a second group of eight was similarly anaesthetized only for the last 2 h of the 6-h period. The steroid-stimulated LH surge was blocked in both groups of rats anaesthetized with alphaxalone. The second experiment involved a comparison of pulsatile LH secretion in animals which were either unanaesthetized (n = 8) or anaesthetized with alphaxalone (n = 9). In six out of nine rats the anaesthetic did not affect the maximum or minimum plasma LH concentrations but significantly slowed the frequency at which LH pulses were measured. In the remaining three anaesthetized rats the drug blocked pulsatile LH secretion. The experiments confirm that some secretion of LH continues during alphaxalone anaesthesia but indicate also that the drug has a more deleterious action upon the oestrogen-stimulated LH surge than believed hitherto. J. Endocr. (1984) 102, 27-31

Dissociation between the ovarian factors controlling sexual receptivity and preovulatory secretion of LH in cyclic female rats

1987 ◽  
Vol 112 (1) ◽  
pp. 133-138 ◽  
Author(s):  
P. Södersten ◽  
P. Eneroth
Keyword(s):  
Sexual Behaviour ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Serum Progesterone ◽  
Lh Surge ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion ◽  
Intact Rats

ABSTRACT Ovariectomy and treatment with oestradiol benzoate (10 μg OB) on the day before behavioural oestrus eliminated the preovulatory surge of LH and reduced the level of sexual receptivity on the following day. Sexual behaviour, but not the LH surge, was restored by progesterone (0·5 mg) given 18 h later. Injection of OB on the day after behavioural oestrus induced a small release of LH and normal sexual behaviour on the following day. Ovariectomy on the day after behavioural oestrus reduced the stimulatory effect of OB on sexual behaviour and eliminated its weakly stimulatory effect on LH release. Sexual behaviour, but not the small LH surge, was restored in these animals by progesterone (0·5 mg) given 18 h later. Treatment of rats ovariectomized 2 days before the day of the LH surge with implants containing oestradiol or injections of oestradiol (1 μg) induced LH surges but the amplitudes of these LH surges were much smaller than those of the normal LH surge. Treatment of intact rats with OB increased serum progesterone levels 24 h later, an effect which was eliminated by ovariectomy. Injections of LH (20 μg) into intact rats on the day after behavioural oestrus also increased serum progesterone concentrations but failed to stimulate sexual behaviour. It is suggested that OB treatment of intact rats on the day after behavioural oestrus stimulates sexual behaviour by inducing a surge of LH secretion which activates ovarian secretion of progesterone. Thus, oestrogen and progesterone but not the LH surge are essential for sexual behaviour. Whereas oestradiol and progesterone restore normal sexual behaviour in ovariectomized rats, additional ovarian factors may be required for induction of normal LH surges. J. Endocr. (1987) 112, 133–138

scholarly journals Effect of androgen on Kiss1 expression and luteinizing hormone release in female rats

2017 ◽  
Vol 233 (3) ◽  
pp. 281-292 ◽  
Author(s):  
Kinuyo Iwata ◽  
Yuyu Kunimura ◽  
Keisuke Matsumoto ◽  
Hitoshi Ozawa
Keyword(s):  
Luteinizing Hormone ◽  
Arcuate Nucleus ◽  
Female Rats ◽  
Hormone Release ◽  
Lh Surge ◽  
Continuous Release ◽  
Ovulatory Dysfunction ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Hyperandrogenic women have various grades of ovulatory dysfunction, which lead to infertility. The purpose of this study was to determine whether chronic exposure to androgen affects the expression of kisspeptin (ovulation and follicle development regulator) or release of luteinizing hormone (LH) in female rats. Weaned females were subcutaneously implanted with 90-day continuous-release pellets of 5α-dihydrotestosterone (DHT) and studied after 10 weeks of age. Number of Kiss1-expressing cells in both the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC) was significantly decreased in ovary-intact DHT rats. Further, an estradiol-induced LH surge was not detected in DHT rats, even though significant differences were not observed between DHT and non-DHT rats with regard to number of AVPV Kiss1-expressing cells or gonadotrophin-releasing hormone (GnRH)-immunoreactive (ir) cells in the presence of high estradiol. Kiss1-expressing and neurokinin B-ir cells were significantly decreased in the ARC of ovariectomized (OVX) DHT rats compared with OVX non-DHT rats; pulsatile LH secretion was also suppressed in these animals. Central injection of kisspeptin-10 or intravenous injection of a GnRH agonist did not affect the LH release in DHT rats. Notably, ARC Kiss1-expressing cells expressed androgen receptors (ARs) in female rats, whereas only a few Kiss1-expressing cells expressed ARs in the AVPV. Collectively, our results suggest excessive androgen suppresses LH surge and pulsatile LH secretion by inhibiting kisspeptin expression in the ARC and disruption at the pituitary level, whereas AVPV kisspeptin neurons appear to be directly unaffected by androgen. Hence, hyperandrogenemia may adversely affect ARC kisspeptin neurons, resulting in anovulation and menstrual irregularities.

scholarly journals Pup removal suppresses estrogen-induced surges of LH secretion and activation of GnRH neurons in lactating rats

2006 ◽  
Vol 191 (1) ◽  
pp. 339-348 ◽  
Author(s):  
Atsushi Fukushima ◽  
Ping Yin ◽  
Maho Ishida ◽  
Nobuhiro Sugiyama ◽  
Jun Arita
Keyword(s):  
Third Ventricle ◽  
Acute Effect ◽  
Suppressive Effect ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Indwelling Catheter ◽  
Lh Surge ◽  
Gnrh Neurons ◽  
Double Immunohistochemical Staining ◽  
Lh Secretion

During lactation, the suckling stimulus exerts profound influences on neuroendocrine regulation in nursing rats. We examined the acute effect of pup removal on the estrogen-induced surge of LH secretion in ovariectomized lactating rats. Lactating and nonlactating cyclic female rats were given an estradiol-containing capsule after ovariectomy, and blood samples were collected through an indwelling catheter for serum LH determinations. In lactating, freely suckled ovariectomized rats, estrogen treatment induced an afternoon LH surge with a magnitude and timing comparable to those seen in nonlactating rats. Removal of pups from the lactating rats at 0900, 1100, or 1300 h, but not at 1500 h, suppressed the estrogen-induced surge that normally occurs in the afternoon of the same day. The suppressive effect of pup removal at 0900 h was completely abolished when the pups were returned by 1400 h. In contrast, pup removal was ineffective in abolishing the stimulatory effect of progesterone on LH surges. Double immunohistochemical staining for gonadotropin-releasing hormone (GnRH) and c-Fos, a marker for neuronal activation, revealed a decrease, concomitantly with the suppression of LH surges, in the number of c-Fos-immunoreactive GnRH neurons in the preoptic regions of nonsuckled rats. An LH surge was restored in nonsuckled rats when 0.1 μg oxytocin was injected into the third ventricle three times at 1-h intervals during pup removal. These results suggest that the GnRH surge generator of lactating rats requires the suckling stimulus that is not involved in nonlactating cyclic female rats.

The inhibitory effect of opiates on gonadotrophin secretion is dependent upon gonadal steroids

1984 ◽  
Vol 102 (2) ◽  
pp. 133-141 ◽  
Author(s):  
R. Bhanot ◽  
M. Wilkinson
Keyword(s):  
Negative Feedback ◽  
Prolactin Secretion ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Inhibitory Effects ◽  
Endogenous Opiates ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Lh Secretion

ABSTRACT We have attempted to clarify the physiological involvement of endogenous opiates in the steroid-mediated control of gonadotrophin release. Our studies showed that there was an acute reduction in the inhibitory effects of endogenous opiates on LH and FSH release following gonadectomy in the rat. This was indicated by a significant reduction in the ability of naloxone to stimulate serum LH/FSH levels (sampled at 15 min) in 26-day-old female rats 48 h after ovariectomy. Luteinizing hormone was highly sensitive to the inhibitory effects of the synthetic met-enkephalin analogue, FK 33-824, at this time (sampled at 90 min). An unexpected observation was that long-term absence of gonadal steroids also disrupted the ability of exogenous opiates, FK 33-824 and morphine, to influence LH release. This was seen as an inability of FK 33-824 (1·0 or 3·0 mg/kg) to inhibit LH secretion. The effects of gonadectomy on opiate control of LH occurred at all developmental stages and were not due to a disruption of sexual maturation. Opiate involvement in prolactin secretion did not appear to be adversely affected by an absence of gonadal steroids. Another novel aspect of this work was that the opiatergic component in the control of gonadotrophin secretion could be reinstated in long-term gonadectomized rats by treatment with oestradiol benzoate or testosterone propionate. Similarly, priming with increasing dosages of oestradiol benzoate which resulted in progressively lower LH levels gave larger naloxone responses. This steroid–opiate interdependency suggests that the negative feedback influence of gonadal steroids on LH secretion is conveyed, in part, by hypothalamic opiate peptides. Our results therefore provide a neurochemical basis for gonadal steroid negative feedback. J. Endocr. (1984) 102, 133–141

scholarly journals SUN-239 Effects of High-Fat Diet-Induced Obesity on Pulsatile LH Secretion and Hypothalamic KISS1 Expression in Female Rats

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Shiori Minabe ◽  
Kinuyo Iwata ◽  
Youki Watanabe ◽  
Hitoshi Ozawa
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Pulse Frequency ◽  
Female Rats ◽  
Standard Diet ◽  
High Fat ◽  
Estrous Cycles ◽  
Menstrual Dysfunction ◽  
Estrous Cyclicity ◽  
Lh Secretion

Abstract Female obesity is associated with menstrual dysfunction leading to anovulation and infertility. It has recently been reported obesity-induced infertility is involved in the dysfunction of a kisspeptin neuron, a key player in reproduction via direct stimulation of gonadotropin releasing hormone (GnRH) and subsequent gonadotropin release in mammalian species. Previous studies reported that obesity due to high-fat diet (HFD) for 8 months induced a disruption in estrous cyclicity, caused by a decrease in Kiss1 (coding kisspeptin) expression in the hypothalamic arcuate nucleus (ARC) in female rodents. Here we showed the effects of shorter-term (4 months) HFD on pulsatile LH secretion and hypothalamic Kiss1 expression to show pathogenic mechanism underlying obesity-induced infertility. Female Wistar-Imamichi strain rats (7 weeks old) fed on either a standard diet (10% calories from fat) or a high-fat diet (45% calories from fat) for 4 months. Estrous cyclicity and body weight were monitored regularly. All animals were implanted with a jugular catheter and collected blood samples to analyze pulsatile LH secretion, after a week of the ovariectomy with low-dose replacement estradiol to negate influence of changes in ovarian steroid levels and mimic diestrous levels of plasma estrogen. On the next day of the blood sampling, rats were perfused with 0.05 M PBS followed by 4% paraformaldehyde and their brains were collected for in situ hybridization of Kiss1 and Gnrh1. The HFD-fed rats showed progressive increases in body weight, along with hyperphagia and adipose tissue accumulation, compared with control animals. Fifty-eight percent of the HFD-fed rats exhibited irregular estrous cycles, whereas remaining HFD-fed rats showed regular cycles. Two out of 7 rats showing HFD-induced irregular estrous cycles exhibited profound suppression of the LH pulse frequency and the number of Kiss1-expressing cells in the ARC, whereas remaining HFD-fed rats showed normal LH pulses and ARC Kiss1 expressions. The number of Kiss1-expressing cells in the ARC had close positive correlation with LH pulse frequency (R2=0.6872, P<0.001) in both groups. Additionally, the number of Kiss1- or Gnrh1-expressing cells in the anteroventral periventricular nucleus or the preoptic area, were comparable between groups. Taken together, our finding reveals the possibility that irregular menstruation was also induced by changes in the kisspeptin-GnRH independent pathway during the incipient stage of obese infertility.

Effects of tamoxifen on concentrations of luteinizing hormone and follicle-stimulating hormone in the plasma of ovariectomized ewes

1983 ◽  
Vol 99 (1) ◽  
pp. 23-29 ◽  
Author(s):  
I. J. Clarke
Keyword(s):  
Plasma Concentrations ◽  
Tamoxifen Treatment ◽  
Similar Response ◽  
Lh Surge ◽  
Peripheral Plasma ◽  
Mediated Effects ◽  
Tamoxifen Citrate ◽  
Oestradiol Benzoate ◽  
Antagonist Action ◽  
Lh Secretion

The effects of tamoxifen on peripheral plasma concentrations of gonadotrophins were studied in ovariectomized ewes. First, ovariectomized ewes were injected (i.m.) with 10 mg tamoxifen citrate/day for 4 days which caused a significant reduction in plasma LH concentrations within 4 days and plasma FSH concentrations within 1 day of the commencement of treatment. Further groups of ovariectomized ewes were then injected (i.m.) with two injections of 10 mg tamoxifen citrate 6 h apart or 20 μg oestradiol benzoate (OB) or tamoxifen citrate plus OB or oil. Tamoxifen treatment caused a reduction in plasma LH and FSH concentrations within 6 h. In four of our ewes receiving OB, a surge in LH secretion was observed; a similar response was observed in two out of four ewes given the combination of tamoxifen citrate and OB. No LH surge was seen in ovariectomized ewes given tamoxifen alone. These results show that tamoxifen reduces plasma gonadotrophin levels in ovariectomized ewes suggesting it is an oestrogen agonist in the sheep pituitary gland. A partial oestrogen antagonist action of tamoxifen is similarly suggested by its ability to block the oestrogen-induced LH surge in some ovariectomized ewes. Since tamoxifen consistently lowers plasma gonadotrophin levels in ovariectomized ewes this could result from action via oestrogen receptors or by central nervous system, non-oestrogen receptor-mediated effects.

Retardation of preovulatory desensitization to negative oestrogen feedback: mechanism of the effect of progesterone in 5-day cyclic rats

1987 ◽  
Vol 114 (3) ◽  
pp. 409-414 ◽  
Author(s):  
F. Döcke ◽  
W. Rohde ◽  
R. Chaoui ◽  
J. Stürzebecher ◽  
G. Dörner
Keyword(s):  
Preoptic Area ◽  
Feedback Mechanism ◽  
Ovarian Cycle ◽  
Female Rats ◽  
Mediobasal Hypothalamus ◽  
Inhibiting Effect ◽  
Gonadotrophin Secretion ◽  
Oestradiol Benzoate ◽  
Lh Secretion ◽  
Follicle Maturation

ABSTRACT Recent studies have shown that oestrogen can induce desensitization to its own gonadotrophin-inhibiting effect in female rats by an action on the medial preoptic area (MPOA). Probably as a consequence of this action, sensitivity to the negative oestrogen feedback declines markedly between metoestrus and dioestrus of the 4-day ovarian cycle. To study this desensitization process in 5-day cyclic rats, females exhibiting regular 5-day vaginal cyclicity were ovariectomized on consecutive days of the cycle, injected with oestradiol benzoate (OB) or oil on the day of ovariectomy and autopsied 24 h after the injection. Estimation of the serum concentration of LH revealed that desensitization to negative oestrogen feedback occurred only between day 2 of dioestrus and pro-oestrus, i.e. 2 days later than in females with a 4-day cycle. In the latter animals, an injection of progesterone in metoestrus or early dioestrus, which induced lengthening of the ovarian cycle for 1 day, delayed the onset of desensitization to a degree similar to that found in spontaneously 5-day cyclic rats. In acutely ovariectomized females, progesterone implants placed in the MPOA, but not those located in the mediobasal hypothalamus, increased the LH-inhibiting effect of low doses of OB. The results suggest that the prolonged secretion of progesterone recorded in 5-day cyclic rats retards follicle maturation and delays the forthcoming ovulation by acting, at least partly, on the MPOA and antagonizing the desensitizing effect of oestrogen. In this way, inhibition of gonadotrophin secretion by oestrogen is enhanced and the increase in tonic LH secretion necessary for the completion of follicle maturation is retarded. J. Endocr. (1987) 114, 409–414

INFLUENCE OF AGE ON THE RELEASE OF LUTEINIZING HORMONE INDUCED BY OESTROGEN AND PROGESTERONE IN IMMATURE RATS

1972 ◽  
Vol 55 (1) ◽  
pp. 97-103 ◽  
Author(s):  
L. CALIGARIS ◽  
J. J. ASTRADA ◽  
S. TALEISNIK
Keyword(s):  
Luteinizing Hormone ◽  
Single Injection ◽  
Significant Rise ◽  
Female Rats ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Old Rats ◽  
Lh Secretion ◽  
Phasic Release

SUMMARY In immature female rats serum luteinizing hormone (LH) concentration, as measured by radioimmunoassay, was found to be higher at 10 or 15 days of age than thereafter. Animals ovariectomized soon after birth or at 5 days of age showed a significant rise in serum LH levels 10 days later. A positive feedback effect on LH secretion was observed on the day following a single injection of oestradiol benzoate (OB) in 28-day-old rats but not in younger animals. However, in animals primed with OB a second dose of OB 2 days later resulted in a significant rise in serum LH levels even in rats of 22 days of age. Progesterone (1 mg) injected 3 days after the injection of a single dose of OB induced, a few hours later, a significant rise in serum LH concentration. This effect was observed from the 22nd day of age but not in younger animals. The magnitude of the response to progesterone, as revealed by the serum LH levels, sharply decreased at the time of puberty. It is concluded that the mechanisms responsible for the tonic release of LH are ready to function at the time of birth or shortly thereafter, while those involved in the phasic release mature around 22 days of age.

Effects of oestradiol benzoate on the pituitary secretion and peripheral kinetics of thyrotrophin in the rat

1985 ◽  
Vol 109 (2) ◽  
pp. 232-236 ◽  
Author(s):  
Rubén Boado ◽  
Susana Deza ◽  
Angel A. Zaninovich
Keyword(s):  
Body Weight ◽  
Turnover Rate ◽  
Serum Levels ◽  
Female Rats ◽  
Distribution Space ◽  
Male And Female Rats ◽  
Oestradiol Benzoate ◽  
Pituitary Secretion ◽  
Kinetics Of ◽  
Peripheral Metabolism

Abstract. Previous works from this laboratory have demonstrated that oestradiol benzoate (EB) in euthyroid male and female rats induced a significant decrease in the pituitary content of TSH while serum levels of this hormone remained normal. The present work studied the effects of EB (25 μg/100 g body weight, during 9 days) on the peripheral metabolism of [125I]rTSH and on the pituitary and plasma concentration of TSH in euthyroid and hypothyroid rats. No significant variations were observed in [125I]rTSH kinetics of EB-treated euthyroid rats vs untreated controls: fractional turnover rate 2.8 ± 0.2 vs 3.0 ± 0.3%/min, distribution space 6.5 ± 0.4 vs 6.8 ± 0.5 ml/100 g body weight, disposal rate 18.4 ± 2.4 vs 18.1 ± 1.9 μU/100 g/min and extrapituitary pool 645 ± 42 vs 614 ± 43 μU/100 g body weight. Similarly, in hypothyroid rats oestrogens induced no changes in TSH kinetics except for an increase in distribution space (P < 0.025). However, oestrogens decreased the pituitary pool of TSH (P < 0.001) in both euthyroid and hypothyroid rats and increased the plasma TSH in hypothyroid animals (P<0.01), all vs their respective controls. Neither hypothyroid group had detectable plasma levels of T4 and T3. In summary: 1) the marked decrease of pituitary TSH with normal plasma TSH induced by EB appears unrelated to the peripheral metabolism of TSH, 2) the results from hypothyroid rats suggest that EB stimulates the release of TSH from the pituitary gland.

PLASMA PROGESTERONE AND ITS RELATIONSHIP TO SERUM GONADOTROPHINS IN IMMATURE FEMALE RATS

1975 ◽  
Vol 64 (2) ◽  
pp. 329-336 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
W. J. DE GREEF ◽  
J.TH.J. UILENBROEK
Keyword(s):  
Body Weight ◽  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Female Rats ◽  
Immature Female ◽  
Plasma Progesterone ◽  
Adult Rat ◽  
Progesterone Treatment ◽  
Serum Luteinizing Hormone ◽  
Oestradiol Benzoate

SUMMARY In immature female rats, low values for concentrations of plasma progesterone were generally found from days 6–15 and from days 25–32 of life. Maximum progesterone concentrations (13·0–14·1 ng/ml), comparable to metoestrous values in the adult rat, occurred on days 20–22. The progesterone appeared to be of ovarian origin since after ovariectomy, on day 18, low progesterone concentrations were found 1 and 2 days later (2·5 ng/ml and 1·3 ng/ml) as compared with control values of 10·7 ng/ml and 14·1 ng/ml. However, adrenalectomy also lowered progesterone concentrations, 1 and 2 days later (6·4 and 4·9 ng/ml). The effect of progesterone, either alone or in combination with oestradiol benzoate (OB), on serum gonadotrophins was studied in rats ovariectomized on day 18. The highest dose of progesterone (0·15 mg) only slightly diminished the rise in serum luteinizing hormone (LH) after ovariectomy and had no effect on serum follicle-stimulating hormone (FSH). Oestradiol benzoate in a dose of 0·025 μg/100 g body weight was highly effective in preventing the rise in both LH and FSH concentrations, and OB treatment (resulting in a near-physiological oestradiol concentration) combined with progesterone treatment was more effective than treatment with OB alone. The results suggest that the amounts of progesterone and oestradiol present in the 20-day-old rat are adequate to cause the decrease in FSH level normally observed in immature female rats around this age.

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