Effect of Antibodies to 17<i>β</i>-Estradiol and Progesterone on the Estrous Cycle of the Rat

Ferin, Michel; Tempone, Antonio; Zimmering, Paula E.; Wiele, Raymond L. Vande

doi:10.1210/endo-85-6-1070

Cited by 198 publications

(62 citation statements)

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“…shed was noted in the present experiment, while no change was observed in a previous report after the administration of estradiol-AS in diestrous rats [13]. Changes in the plasma inhibin concentrations seemed to reflect the delay of ovulation and an increase in the number of mature follicles just before the delayed LH surge.…”

Section: Discussioncontrasting

confidence: 79%

“…This effect was previously observed using antiserum against estradiol [13,14]. In an experiment performed by Ferin et al (1969) [13], in estradiol-AS injected rats the LH surge was delayed and their estrous cycle prolonged by 4 days. When diethylstilbestrol, a non-steroidal estrogen, was given to estradiol-AS treated rats, the LH surge occurred at the expected time [14].…”

Section: Discussionsupporting

confidence: 62%

“…estradiol is known to induce gonadotropin surges in intact cyclic rats [13][14][15] or in ovariectomized rats [16][17][18][19][20][21]. However, the preceding experiments, for the most part, have been carried out using ovariectomized rats or the pituitary cell culture system, and they have not completely specified whether or not estradiol physiologically suppresses FSH secretion in the cyclic female rat as inhibin does [22].…”

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confidence: 99%

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Effects of Passive Immunization Against Estradiol on LH and FSH in the Diestrous Female Rat.

Arai

Watanabe

Taya

et al. 1996

Journal of Reproduction and Development

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Abstract. The role of estradiol in regulating the secretion of LH and FSH from diestrus to proestrus of rats was examined by neutralizing estradiol using antiserum against estradiol (estradiol-AS). An IV injection of varying doses of estradiol-AS at 1100 h on diestrus caused a significant rise in plasma LH (maximally 318.2 ± 27.3% vs control) and non-significant rise in plasma FSH (maximally 144.0 ± 22.0% vs control) at 6 hours after the injection. Administration of the antiserum prolonged the estrous cycle and the day of ovulation by 1 day. The prolongation was caused by a 1-day delay of the LH surge. A small but significant increase in the number of tubal oocytes shed was noted in the estradiol-AS treated group (16.3 ± 0.8, n=12) compared with controls (14.5 ± 0.4, n=15). These results indicated that estradiol suppresses tonic secretion of LH and that the steroid may also be concerned with the regulation of FSH. They also confirmed that the rise in plasma estradiol from diestrous morning is necessary for triggering the LH surge on the following afternoon. Further, administration of estradiol-AS on diestrus resulted in a significant increase in the number of oocytes shed, probably due to the increase in tonic secretion of LH and FSH between diestrus to proestrus. Key words: Estradiol, Immunoneutralization, LH, FSH, Diestrous rat.(J. Reprod. Dev. 42: [185][186][187][188][189][190][191] 1996) Accepted for publication: April 20, 1996 Correspondence: K. Taya t is generally accepted that estradiol affects LH and FSH secretion. Many investigations have estradiol is known to induce gonadotropin surges in intact cyclic rats [13][14][15] or in ovariectomized rats [16][17][18][19][20][21]. However, the preceding experiments, for the most part, have been carried out using ovariectomized rats or the pituitary cell culture system, and they have not completely specified whether or not estradiol physiologically suppresses FSH secretion in the cyclic female rat as inhibin does [22]. To specify the physiological roles of estradiol in the regulation of FSH and LH secretion, passive immunization against estradiol was carried out in the cyclic female rat. The present experiment was undertaken to examine the effects of immunoneutralization of estradiol on LH, FSH, inhibin and progesterone levels in plasma, on LH and FSH levels in the pituitary gland, and on ovulation. Attention was focused on the diestrous morning, Iensured to determine the role of estradiol in the regulation of gonadotropin secretion. An administration of estradiol benzoate lowers plasma concentrations of gonadotropins elevated in longterm ovariectomized rats [1], and estradiol completely suppresses the increase in LH secretion [2-4] and partially suppresses the FSH secretion [3,4] after ovariectomy. Estradiol also modulates gonadotropin secretion and gonadotropin gene expression by direct action on gonadotropes or by altering gonadotropin releasing hormone (GnRH) secretion [5][6][7][8][9][10][11][12]. Further,

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Section: Discussioncontrasting

confidence: 79%

Section: Discussionsupporting

confidence: 62%

mentioning

confidence: 99%

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Effects of Passive Immunization Against Estradiol on LH and FSH in the Diestrous Female Rat.

Arai

Watanabe

Taya

et al. 1996

Journal of Reproduction and Development

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“…The mechanism of estrogen positive feedback has remained elusive, but several components are known. First, high levels of estradiol are absolutely essential (Brom and Schwartz, 1968;Ferin et al, 1969;Labhsetwar, 1970). Second, estradiol induced progesterone receptors (PR) in the hypothalamus are needed (Chappell et al, 2000;DePaolo, 1988;Hibbert et al, 1996;Mahesh and Brann, 1992;SanchezCriado et al, 1994;Snyder et al, 1984).…”

Section: Model Of Estrogen Positive Feedbackmentioning

confidence: 99%

Estradiol regulation of progesterone synthesis in the brain

Micevych

Sinchak

2008

Molecular and Cellular Endocrinology

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Steroidogenesis is now recognized as a global phenomenon in the brain, but how it is regulated and its relationship to circulating steroids of peripheral origin have remained more elusive issues. Neurosteroids, steroids synthesized de novo in nervous tissue, have a large range of actions in the brain, but it is only recently that the role of neuroprogesterone in the regulation of arguably the quintessential steroid dependent neural activity, regulation of the reproduction has been appreciated. Circuits involved in controlling the LH surge and sexual behaviors were thought to be influenced by estradiol and progesterone synthesized in the ovary and perhaps the adrenal. It is now apparent that estradiol of ovarian origin regulates the synthesis of neuroprogesterone, and it is the locally produced neuroprogesterone that is involved in the initiation of the LH surge and subsequent ovulation. In this model, estradiol induces the transcription of progesterone receptors while stimulating synthesis of neuroprogesterone. Although the complete signaling cascade has not been elucidated, many of the features have been characterized. The synthesis of neuroprogesterone occurs primarily in astrocytes and requires the interaction of membrane associated estrogen receptor-α with metabotropic glutamate receptor-1a. This G protein-coupled receptor activates a phospholipase C that in turn increases inositol trisphosphate (IP 3 ) levels mediating the release of intracellular stores of Ca 2+ via an IP 3 receptor gated Ca +2 channel. The large increase in free cytoplasmic Ca 2+ ([Ca 2+ ] i ) stimulates the synthesis of progesterone, which can then diffuse out of the astrocyte and activate estradiol-induced progesterone receptors in local neurons to trigger the neural cascade to produce the LH surge. Thus, it is a cooperative action of astrocytes and neurons that is needed for estrogen positive feedback and stimulation of the LH surge.

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“…The most inter¬ esting feature of these observations is that oestrogen-induced surges of LH were observed only in the afternoon of pro-oestrus, suggesting the involvement of a 'CNS clock'. Since the LH surge can be blocked by the administration of antibodies to oestradiol-17ß (Ferin, Tempone, Zimmering & Van de Wiele, 1969), it was proposed that, in the rat, ovarian oestradiol determines the day of the surge while the CNS determines its hour of onset (Bogdanove, 1972).…”

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confidence: 99%

Regulation of the hypothalamic-pituitary-ovarian axis in women

Yen¹

1977

Reproduction

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Summary. To (1932) proposed that sex steroids influence gonadotrophin secretion not only by negative feedback (inhibition) but also by positive (stimulating) feedback and that these effects are mediated through a 'sex centre' in the central nervous system. These early observations and concepts are fundamental to the many subsequent studies on pituitary regulation and to the recent advances made in the understanding of the interplay among the elements of the CNS-pituitary-ovarian system in the regulation of cyclic gonadotrophin secretion in women.The operating characteristics of the hypothalamic-pituitary-ovarian (H-P-O) axis are complex and the cellular and subcellular mechanism(s) governing interaction of the several components of the system are far from understood. Even so, an understanding of the performance of a system may be achieved by determining the relationship between the output as a function of changing input. Unlike other pituitary and target organ systems, the H-P-O system involves multiple trophic hor¬ mones with different biological actions (e.g. FSH and LH) and multiple target hormones having nonlinear feedback functions. It is the purpose of this review to provide a brief account of the opera¬ ting characteristics of the elements of the H-P-O system and to attempt to assemble these elements into a functionally coherent system for controlling the cyclic release of gonadotrophin. The ovaryThe endocrine components of the ovary The ovary, inherently a cyclic organ, is composed of two endocrine structures which are morpho¬ logically and functionally related : the follicular complex and the corpus luteum. They have sequential

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Effect of Antibodies to 17β-Estradiol and Progesterone on the Estrous Cycle of the Rat

Cited by 198 publications

References 0 publications

Effects of Passive Immunization Against Estradiol on LH and FSH in the Diestrous Female Rat.

Effects of Passive Immunization Against Estradiol on LH and FSH in the Diestrous Female Rat.

Estradiol regulation of progesterone synthesis in the brain

Regulation of the hypothalamic-pituitary-ovarian axis in women

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