Prolonged Neonatal Exposure to Estrogen Inhibits Pulsatile LH Release and Estrous Cyclicity in Female Rats Probably Via Disruption of the Arcuate Metastin/Kisspeptin Neurons.

Changes in the characteristics of LH secretory pulses in female rats were determined in different hormonal conditions; during the oestrous cycle and after ovariectomy and oestrogen treatment. The frequency and amplitude of the LH pulses were stable during the oestrous cycle except at oestrus when a pattern could not be discerned because of low LH concentrations. These were significantly lower than those measured during other stages of the cycle. Mean LH concentrations and LH pulse amplitudes increased with time up to 30 days after ovariectomy. The frequency of the LH pulse was unchanged 4 days after ovariectomy when mean LH levels had already increased. The frequency increased 10 days after ovariectomy and then remained stable in spite of a further increase in mean serum LH concentrations. Oestradiol-17β injected into ovariectomized rats caused a decrease in LH pulse amplitude but no change in pulse frequency. One day after treatment with oestradiol benzoate no LH pulse was detectable, probably because the amplitude was too small. A generator of pulsatile LH release is postulated and an oestrogen effect on its function is discussed.

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Effect of low doses of continuously administered catecholoestrogens on peripheral and central target organs

Acta Endocrinologica ◽

10.1530/acta.0.0960470 ◽

1981 ◽

Vol 96 (4) ◽

pp. 470-474 ◽

Cited By ~ 8

Author(s):

Peter Ball ◽

Günter Emons ◽

Ulrich Gethmann

Keyword(s):

Serum Levels ◽

Female Rats ◽

Low Doses ◽

Vaginal Opening ◽

Uterine Weight ◽

Central Target ◽

Male And Female Rats ◽

Target Organs ◽

Uterine Growth ◽

Lh Release

Abstract. Osmotic minipumps containing low doses of either 4-hydroxyoestradiol or 2-hydroxyoestradiol2) were sc implanted for 152 h (6⅓ day) into immature male and female rats. At the end of the test period the animals were killed and the uterine weight, the vaginal opening, the gonadotrophin serum levels and the gonadal weight monitored. The following results were obtained: 1) a significant increase in the uterine weight and a consistent vaginal opening were observed after 4-hydroxyoestradiol but not after 2-hydroxyoestradiol treatment, 2) LH-levels increased after 2-hydroxyoestradiol but not after 4-hydroxyoestradiol; the increase was, however, not significant, 3) FSH-levels and gonadal weights were lowered by 4-hydroxyoestradiol treatment in male animals only; 2-hydroxyoestradiol had no effect on FSH-levels in both sexes, 4) in no instance an antioestrogenic effect of either catecholoestrogen was observed. It is concluded that 4-hydroxyoestrogens — using the above paradigm — have a significant importance on uterine growth and vaginal opening but (on day 6) no role on LH-release, whereas 2-hydroxyoestrogens may increase LH levels (on day 6) but are nearly ineffective with respect to peripheral parameters.

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Neonatal exposure to estradiol-17β modulates tumour necrosis factor alpha and cyclooxygenase-2 expression in brain and also in ovaries of adult female rats

Hormone Molecular Biology and Clinical Investigation ◽

10.1515/hmbci-2015-0072 ◽

2016 ◽

Vol 25 (2) ◽

Author(s):

Radhika Nagamangalam Shridharan ◽

Harshini Krishnagiri ◽

Vijayakumar Govindaraj ◽

SitiKantha Sarangi ◽

Addicam Jagannadha Rao

Keyword(s):

Recent Observation ◽

Endocrine Disrupting Compounds ◽

Perinatal Period ◽

Female Rats ◽

Neonatal Exposure ◽

Sexually Dimorphic ◽

Necrosis Factor Alpha ◽

Factor Alpha ◽

And Behavior ◽

Estradiol 17Β

AbstractThe sexually dimorphic organization in perinatal rat brain is influenced by steroid hormones. Exposure to high levels of estrogen or endocrine-disrupting compounds during perinatal period may perturb this process, resulting in compromised reproductive physiology and behavior as observed in adult In our recent observation neonatal exposure of the female rats to estradiol-17β resulted in down-regulation of

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

Journal of Endocrinology ◽

10.1530/joe-16-0568 ◽

2017 ◽

Vol 233 (3) ◽

pp. 281-292 ◽

Cited By ~ 8

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.

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Neonatal exposure to bisphenol A alters the hypothalamic-pituitary-thyroid axis in female rats

Toxicology Letters ◽

10.1016/j.toxlet.2017.12.029 ◽

2018 ◽

Vol 285 ◽

pp. 81-86 ◽

Cited By ~ 17

Author(s):

Marina O. Fernandez ◽

Nadia S. Bourguignon ◽

Paula Arocena ◽

Matías Rosa ◽

Carlos Libertun ◽

...

Keyword(s):

Bisphenol A ◽

Female Rats ◽

Neonatal Exposure ◽

Pituitary Thyroid Axis ◽

Thyroid Axis

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Reproductive effects in male and female rats from neonatal exposure to p-octylphenol

Reproductive Toxicology ◽

10.1016/s0890-6238(01)00173-3 ◽

2001 ◽

Vol 15 (6) ◽

pp. 683-692 ◽

Cited By ~ 31

Author(s):

T Nagao ◽

S Yoshimura ◽

Y Saito ◽

M Nakagomi ◽

K Usumi ◽

...

Keyword(s):

Female Rats ◽

Neonatal Exposure ◽

Male And Female ◽

Reproductive Effects ◽

Male And Female Rats

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Involvement of norepinephrine in pituitary LH release induced by oestradiol in vitro

Acta Endocrinologica ◽

10.1530/acta.0.1070199 ◽

1984 ◽

Vol 107 (2) ◽

pp. 199-203

Author(s):

A. Miyake ◽

K. Tasaka ◽

T. Aono

Keyword(s):

Oestrous Cycle ◽

Female Rats ◽

Direct Effects ◽

Significant Release ◽

Lh Release ◽

Lh Secretion ◽

Perifusion System ◽

Double Chamber

Abstract. The direct effects of oestradiol-17β (E2) on pituitary luteinizing hormone (LH) release and the role of norepinephrine (NE) in E2-induced gonadtrophin release were examined in a sequential double chamber perifusion system by perifusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normally cycling female rats. Administration of E2 induced significant release (70–160% increase, P < 0.05) of LH from the pituitary of rats in pro-oestrus, but not in other stages of the oestrous cycle. When the MBH and the pituitary were perifused in sequence, E2 induced significant release of LH in all stages of the oestrous cycle except oestrus. When the pituitary from rats in dioestrus II was perifused alone with medium containing 200 ng/ml NE, significant release of LH (80–170% increase, P < 0.05) was observed after the administration of E2. The E2-induced LH release in pro-oestrus was completely abolished by perifusion with medium containing diethyldithiocarbamate, an inhibitor of NE synthesis. These findings suggest that NE may be involved in changes of pituitary responsiveness in LH secretion to oestrogen during the rat oestrous cycle.

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Abnormal Response of the Neuropeptide Y-Deficient Mouse Reproductive Axis to Food Deprivation But Not Lactation

Endocrinology ◽

10.1210/en.2002-221024 ◽

2003 ◽

Vol 144 (5) ◽

pp. 1780-1786 ◽

Cited By ~ 23

Author(s):

Jennifer W. Hill ◽

Jon E. Levine

Keyword(s):

Neuropeptide Y ◽

Food Consumption ◽

Food Deprivation ◽

Normal Female ◽

Estrous Cycles ◽

Energy Deficiency ◽

Steroid Dependent ◽

Reproductive Axis ◽

Estrous Cyclicity ◽

Lh Release

Neuropeptide Y (NPY) plays a key role in both food intake and GnRH secretion. Food deprivation elevates hypothalamic NPY activity and suppresses LH and gonadal steroid secretion. Similarly, lactation up-regulates NPY expression as food consumption increases and estrous cycles cease. These observations suggest that NPY coordinates reproductive suppression in response to energy deficiency; if so, the reproductive axis of NPY knockout (KO) mice should be impervious to lactation and food deprivation. We monitored food consumption, body weight, and estrous cyclicity during lactation in NPY KO mice with large and small litters. NPY KO mice with either litter size resembled wild types (WTs) in weight regulation and food consumption. Large-litter mothers had longer anestrous periods and smaller pups at weaning, but NPY KOs and WTs did not differ in either respect. We also examined the LH response of NPY KO mice to 48 h without food. Basal levels of LH in ovariectomized NPY KO animals decreased in response to fasting, but LH levels in intact and estrogen-treated ovariectomized NPY KO animals did not. In contrast, WTs consistently showed fasting-induced suppression of LH. Our findings suggest that other systems can sustain the hyperphagia of lactation and NPY alone is not responsible for suppressing cyclicity during lactation. Nevertheless, the suppression of basal LH release that accompanies food deprivation in normal female mice appears to require the steroid-dependent actions of NPY.

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Effects of acute administration of 2-hydroxylated metabolites of oestrogens on LH and prolactin secretion in male and female prepubertal rats

Journal of Endocrinology ◽

10.1677/joe.0.1030317 ◽

1984 ◽

Vol 103 (3) ◽

pp. 317-325

Author(s):

A. K. Brar ◽

G. Fink

Keyword(s):

Plasma Concentration ◽

Female Rats ◽

Male Rats ◽

Male Rat ◽

Female Rat ◽

Uterine Weight ◽

Immature Female ◽

Male And Female ◽

Immature Male ◽

Lh Release

ABSTRACT The effects of catechol oestradiol and catechol oestrone on the release of LH and prolactin were investigated in immature male and female Wistar rats. In male rats both catechol oestradiol and catechol oestrone significantly increased the plasma concentration of LH, and catechol oestradiol but not catechol oestrone significantly increased the plasma concentration of prolactin and decreased the pituitary concentration of LH. The parent oestrogens, oestradiol-17β and oestrone, had no effect on plasma LH concentrations, but both increased significantly the plasma concentration of prolactin, and oestrone but not oestradiol-17β increased the pituitary concentration of LH. In immature female rats, catechol oestradiol inhibited the surge of LH and the increase in uterine weight induced by injecting pregnant mare serum gonadotrophin (PMSG). The injection of oestrone induced an increase in the plasma concentration of LH which was about nine times greater than that produced by oestradiol-17β. There were no significant differences in the effects of these steroids on plasma prolactin concentration. These results (i) confirm that in the immature male rat catechol oestrogens can stimulate LH release and show that catechol oestradiol can increase prolactin release, (ii) show that catechol oestradiol can inhibit the stimulatory effects of PMSG on LH release and uterine weight in the immature female rat, and (iii) demonstrate that oestrone can stimulate LH release in the immature female rat. J. Endocr. (1984) 103, 317-325

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Differential effects of forskolin on LH and GH release

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1985.249.4.e392 ◽

1985 ◽

Vol 249 (4) ◽

pp. E392-E397

Author(s):

W. S. Evans ◽

T. H. Brannagan ◽

E. R. Limber ◽

M. J. Cronin ◽

A. D. Rogol ◽

...

Keyword(s):

Growth Hormone ◽

Anterior Pituitary ◽

Gonadotropin Releasing Hormone ◽

Female Rats ◽

Second Phase ◽

Pituitary Cells ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Lh Release ◽

Biphasic Release

The effects of forskolin, an agent which increases intracellular levels of cAMP, on basal luteinizing hormone (LH) and growth hormone (GH) release and on gonadotropin-releasing hormone (GnRH)-stimulated LH release were documented. Continuously perifused dispersed anterior pituitary cells from female rats at random stages of the estrous cycle were used. Secretory rates of both LH and GH increased in a concentration-dependent manner in response to a 1-h challenge with 0.03, 0.1, 0.3, 1, or 3 microM forskolin. In response to 0.3 microM forskolin, maximum GH release was achieved within 15-20 min, after which secretion decreased. In contrast, LH release increased gradually, became maximal at 1.5-2 h, and remained constant until the forskolin was withdrawn. Cells exposed to 10 nM GnRH for 4 h exhibited a biphasic release of LH with the interphase nadir occurring at 30 min. The second phase of LH release was enhanced by simultaneous addition of forskolin with the GnRH. Whereas second phase release did not increase further, exposure of the cells to forskolin for 60 or 120 min before GnRH resulted in increased first-phase LH release. We suggest that, whereas our data are consistent with a role for cAMP in mediating the acute release of GH, cAMP may be involved in the process through which nonimmediately releasable LH becomes available for release.

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