Stimulatory Feedback Action of Estradiol in Intact and Ovariectomized Lactating Rats1

Coppings, R. J.; McCann, Samuel M.

doi:10.1095/biolreprod21.1.219

Cited by 14 publications

(7 citation statements)

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“…It is well established that chronic progesterone exposure or progesterone administration before oestrogen administration blocks the oestrogen‐induced surge in ovariectomized virgin females (9, 10). Furthermore, although the ability of exogenous oestrogen administration to stimulate an LH surge is attenuated in ad libitum fed lactating rats, responsivity to oestrogen is partially restored by ovariectomy on days 1–2 postpartum (11–13).…”

mentioning

confidence: 99%

Food Restriction During Lactation Results in Prolonged Hyposensitivity to the Positive‐Feedback Effects of Oestradiol

Abizaid

Woodside

2003

J Neuroendocrinology

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Food restriction prolongs lactational infertility in rats. Here, we investigated whether an attenuated response to the positive-feedback effects of oestrogen on luteinizing hormone release contributed to this effect. The ability of oestrogen to induce surges in luteinizing hormone in ad libitum fed and food-restricted dams at different times of lactation was compared. The results showed that, on day 20 postpartum, ad libitum fed dams showed luteinizing hormone surges after oestrogen treatment, but food-restricted dams did not. Ovariectomy or RU486 treatment restored the ability of oestrogen to induce luteinizing hormone surges in food-restricted dams, and chronic progesterone exposure reduced oestrogen-induced surges of luteinizing hormone in ad libitum fed ovariectomized dams. Food restriction also resulted in a reduced ability of oestrogen to induce progesterone receptor immunoreactivity, but did not reduce the number of oestrogen receptors (ERalpha) in the anteroventralperiventricular area. As with the surge in luteinizing hormone, the effects of food restriction on oestrogen induction of progesterone receptors were mediated by progesterone. Together, these results suggest that the ability of food restriction to extend the length of lactational diestrus is mediated, in part, by a decrease in sensitivity to the positive-feedback effects of oestrogen. This results from high circulating concentrations of progesterone which apparently reduce the ability of oestrogen to induce progesterone receptor expression.

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mentioning

confidence: 99%

Food Restriction During Lactation Results in Prolonged Hyposensitivity to the Positive‐Feedback Effects of Oestradiol

Abizaid

Woodside

2003

J Neuroendocrinology

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“…The essential role of the suckling stimulus in the estrogeninduced LH surge in lactating rats contrasts surprisingly with its inhibitory effect on pulsatile LH secretion (Hammons et al 1973, Smith & Neill 1977, Smith 1978a, Maeda et al 1989 and the estrogen-induced LH surge in ovariectomized lactating rats (Coppings & McCann 1979, Tsukamura et al 1988 as shown by previous studies. Experiments in which the times of initiation and termination of pup removal were varied indicate that the LH surge is blocked if pups are removed during a period starting immediately before the initiation of the estrogen-induced LH surge, and continuing throughout the occurrence of the surge.…”

Section: Discussionmentioning

confidence: 87%

“…During early lactation, this inhibition is mainly due to the suckling stimulus itself rather than the high prolactin levels caused by the suckling stimulus (Lu et al 1976, Smith 1978b. Furthermore, even though estrogen treatment can induce daily LH surges in lactating ovariectomized rats (Smith 1978b, Coppings & McCann 1979, the magnitudes of the daily surges in lactating rats have been found to decline more rapidly than in nonlactating rats (Coppings & McCann 1979, Tsukamura et al 1988.…”

Section: Introductionmentioning

confidence: 99%

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

Fukushima¹,

Yin²,

Ishida³

et al. 2006

Journal of Endocrinology

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During lactation, the suckling stimulus exerts profound influences on neuroendocrine regulation in nursing rats. We examined the acute effect of pup removal on the estrogeninduced 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 gonadotropinreleasing 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 mg 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.

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“…During the first stages of lactation, estradiol levels are low, in later stages when the suckling stimulus decreases and PRL and progesterone levels de cline, estradiol titers increase to finally attain preovulato ry levels on the first proestrus after lactational infertility [11,12], Estradiol action to stimulate LH surges is exerted on the central nervous system facilitating the release of surge amounts of GnRH and, at the same time, at the adenophypophyseal gland amplifying GnRH action [13]. It has been argued that the feedback mechanism by which estradiol induces an LH surge is intact in lactating rats [14]; though, on the other hand, it has been suggested that during lactation the hypothalamic-pituitary system is rel atively insensitive to the positive feedback effect of estro gen [15,16]. In previous studies we demonstrated that ovarian FSH receptors increased in the first ovulatory cycle after lactational infertility [8], The present work was designed to evaluate the contribution of anterior pituitary estradiol receptors in ovulation induction by midlactation pup removal.…”

Section: Introductionmentioning

confidence: 99%

Anterior Pituitary Estradiol Receptors Associated with the Reinstatement of Ovulatory Cycles after Lactation Interruption in the Rat

Lux‐Lantos

Hockl²,

Tesone³

et al. 1994

Neuroendocrinology

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The participation of adenohypophyseal estradiol receptors in the reinstatement of ovulatory cycles after lactation interruption was investigated. In rats whose pups were removed on day 13 postpartum (LRX), prolactin levels fell as from 1600 h on the same day, estradiol peaked on the morning of day 15 and gonadotropins and prolactin (PRL) surged on the afternoon of day 15. No significant changes in gonadotropins or estradiol levels were observed in rats which remained with their litters (LRP); in these rats daily afternoon surges of PRL were detected. No significant variations in anterior pituitary nuclear or cytosolic estradiol receptors were determined in LRP rats. In the nuclear fraction of LRX rats, an important increase (430.8 ± 124.9%) in receptor titers was observed on day 15. In these animals a significant increase (34.8 ± 1.3%) in cytosolic estradiol receptors was observed on day 14, followed by a fall on day 15 (–31.6 ± 6.6%) in comparison to day 13 levels. The receptor variations observed on day 15 closely resemble estrous cyclic changes determined in adult females. However, an observation which does not resemble those cycle variations is the increase in cytosolic receptors observed on day 14 in LRX rats. This increase may be the consequence of a decrease in dopamine levels induced by pup removal. To our knowledge this is the first time that the involvement of pituitary estradiol receptors in the reinstatement of ovulatory cycles after lactation interruption has been described.

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Stimulatory Feedback Action of Estradiol in Intact and Ovariectomized Lactating Rats1

Cited by 14 publications

References 0 publications

Food Restriction During Lactation Results in Prolonged Hyposensitivity to the Positive‐Feedback Effects of Oestradiol

Food Restriction During Lactation Results in Prolonged Hyposensitivity to the Positive‐Feedback Effects of Oestradiol

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

Anterior Pituitary Estradiol Receptors Associated with the Reinstatement of Ovulatory Cycles after Lactation Interruption in the Rat

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