Positive Feedback Sites of Estrogen in the Brain on Ovulation

Terasawa, Ei; Kawakami, Michiyuki

doi:10.1507/endocrj1954.21.51

Cited by 33 publications

(3 citation statements)

References 8 publications

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“…These findings point out that the extrahypothalamic areas other than the SEPT and the MPO are the primary feedback site of EB to stimulate early ovulatory gonadotropin release. This is supported by the fact that EB injection simultaneous with the MPO roof cut could not advance ovulation in the present experiment and in the study of Terasawa and Kawakami (1974). There is considerable evidence that the ARC median eminence region (ME) is a site for positive beedback action of estrogen.…”

Section: Discussionsupporting

confidence: 71%

Localization and Mechanism of Stimulatory Feedback Action of Estrogen: Effect of Limbic Forebrain Implantation of Estradiol Benzoate on Advancement of Ovulation

1975

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SynopsisThe sites and mechanism of the ovulation-inducing action of estradiol benzoate (EB) were studied by brain implantation of the crystalline steroid through chronically implanted outer cannula at 12: 00 on diestrus day 2 in the 5-day cyclic rat. EB implantation in the medial amygdala or the bed nucleus of stria terminalis advanced cyclic changes in vaginal smears, timing of ovulatory LH release, and ovulation by 1 day, resulting in 4-day cycle. When implants in the bed nucleus of stria terminalis were placed for a shorter period of time on diestrus day 2, from 12: 00 to 20: 00, advancement of these parameters were similarly observed.Serum concentration of FSH and that of prolactin were significantly elevated at 20: 00 on the same day in the rats implanted with EB in the medial amygdala or the bed nucleus of stria terminalis, compared with those in the non-treated controls. LH was not affected. The implantation in the arcuate nucleus was also effective to advance ovulation, but the anterior deafferentation prevented the effect. In contrast, EB implantation in the medial septal nucleus, the medial preoptic area, or the medial basal prechiasmatic area was consistently ineffective to advance vaginal cycle and ovulation. Multiunit activity in the arcuate nucleus showed an afternoon elevation on the day of implantation in these areas and as well on the day following, while it did not show such elevation on the day of impalntation in the medial preoptic area. It is concluded that EB acts on the medial amygdala and the bed nucleus of stria termianlis in the mid-diestrus in 5-day cycle to stimulate FSH and prolactin release without affecting LH, which changes trigger a chain of reproductive events inducing early release of ovarian steroid responsible for early ovulatory gonadotropin release. The arcuate nucleus in one of the sites of stimulatory action of estrogen, but it requires the neural influence presumably from the medial amygdala and the bed nucleus of stria terminalis via the preoptic area for stimulating the ovulatory hormone release. EB exposure is considered to be endowed with the increase of its resposibility to this neural influence.

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Section: Discussionsupporting

confidence: 71%

Localization and Mechanism of Stimulatory Feedback Action of Estrogen: Effect of Limbic Forebrain Implantation of Estradiol Benzoate on Advancement of Ovulation

1975

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“…In fact, several investigations have shown this area and/or the stria terminalis as the most important structure in conducting the amygdalar impulses for stimulating goandotropin release to the hypothalamus. The destruction of the BST or the stria terminalis on the morning of proestrus blocked spontaneous ovulation (Velasco and Taleisnik, 1971;Kawakami and Terasawa, 1972), and also annulled the effect of amygdalar stimulation or amygdalar implantation of estrogen to induce ovulation (Velasco and Taleisnik, 1969;Terasawa and Kawakami, 1974).…”

Section: Discussionmentioning

confidence: 99%

Study on the Bed Nucleus of Stria Terminalis in Relation to Gonadotropin Control

Kawakami

Kimura

1974

Endocrinol Japon

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SynopsisRole of the bed nucleus of stria terminalis (BST) in the control of gonadotropin release in the female rat was studied.Electrical stimulation of the BST on the day of diestrus II increased the serum concentration of FSH, but not of LH. The stimulation on the day of estrus increased serum concentration of LH as well as on the day of proestrus. In the ovariectomized and estrogen-treated rat, the stimulation decreased serum concentration of FSH; but in the ovariectomized and progesterone-treated rat the stimulation did not decrease it. Implantation of estrogen into the BST inhibited th castration-induced increase of LH and FSH in serum.These results indicate that the BST is one of negative feedback sites of estrogen, and probably participates in folliculotropin secretion which is responsible for estrogen secretion before proestrus. The physiological significance of its ability to induce LH release on the day of estrus in response to stimulation is not known now.It was firstly introduced by Everett et al. (1964) that the septal complex participates in the control of reproductive function in the rat. We observed that the multiple unit activity in the bed nucleus of the stria terminalis (BST) showed a characteristic elevated pattern during the critical period on the day of proestrus and that electrochemical stimulation of this area induced ovulation in the pentobarbital-blocked proestrous rat (Kawakami et al., 1970).From the succeeding experiments, further informations on the BST have been abailable; the acute destruction of the BST in the afternoon of diestrus I prevented uterine and vaginal changes which should be observed on the day of proestrus (Kawakami and Terasawa, 1972), and the chronic destruction resulted in a decrease of pituitary and serum contents of FSH on the day of diestrus II (Kawakami et al., 1973b). These facts indicated us that the BST is not only involved in the triggering mechanisms of LH surge on the day of proestrus, but also in the gonadotropin secretion to stimulate follicular growth and steroidgenesis before proestrus.The present experiment was undertaken to confirm this supposition, and furthermore to determine the attitude to estrogen, in relation to gonadotropin release. Materials and MethodsAdult female Wistar rats were housed in an airconditioned room with artificial light from 5:00 to 19:00, and maintained with ordinary laboratory chow and water ad libitum. Vaginal smears were taken daily around 10:00 and only rats showing at least consecutive 4-day cycles were used. Some rats were ovariectomized at various periods before the experiments,

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“…Lesion and electrical stimulation studies originally pointed to the POAi AH as crucial to the induction of the LH surge [Hillarp, 1949;Halasz and Gorski, 1967: Everett and Radford, 19611. Although early studies on the effects of implantation of small quantities of steroid into the CNS were confusing and fraught with artifact [Palka et al, 1966;Docke and Dorner , 1965;Weick and Davidson, 1970;Terasawa and Kawakami, 1974;Billard and McDonald, 19731, more recently, carefully controlled implantation experiments have provided strong support for the POAi AH as the site of estradiol's positive feedback effects [Goodman, 1978b3. Although estradiol will increase the responsiveness of the pituitary to LHRH and so contribute to positive feedback, in the rat this effect is neither sufficient nor necessary for the LH surge [Fink 1979;Levine and Ramirez, 19821. The mechanism by which estradiol acts in the central nervous system (CNS) and the pituitary to produce effects on serum LH is thought to involve the estrogen receptor.…”

Section: Introductionmentioning

confidence: 99%

Differential sensitivity of estrogen target tissues: Implications for estrogen regulation of serum luteinizing hormone

Kelner

Peck

1984

J of Neuroscience Research

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In the rat, it is generally accepted that the primary site of estrogen's stimulatory (positive) effects on serum LH is the preoptic area-anterior hypothalamus (POA/AH). In contrast, the primary site of estrogen's inhibitory (negative) effects on serum LH levels has not been conclusively identified. There is evidence to suggest both a medial basal hypothalamic (MBH) and an anterior pituitary site of action. The present studies utilized a unique characteristic of these estrogen effects to investigate their putative loci. Extensive dose-response curves of estrogen's induction of positive and negative feedback indicated that the negative feedback response was activated at a lower concentration of serum estradiol than the positive feedback response. The differential sensitivities of these two responses suggested that the tissues mediating them might also be differentially sensitive to estradiol. In a previous paper, we showed that receptor translocation is an index of estrogen sensitivity. We measured receptor translocation in response to a series of estradiol doses in the POA/AH, the MBH, and the pituitary. Dose-response curves for estrogen's effect on receptor translocation showed that the pituitary receptor translocation mechanism is activated at significantly lower levels of serum estradiol than that of either the POA/AH or the MBH. These results are consistent with the POA/AH as a site of estrogen's positive feedback effects. In addition, they suggest that negative feedback in the rat may be mediated via estrogen's action at the anterior pituitary. Estrogen's negative feedback effect on serum LH occurs at a serum level of estrogen at which no receptor is translocated in the MBH. Therefore, the pituitary, which does possess nuclear receptors at these estradiol dose levels, is more likely to be the primary mediator of estrogen's negative feedback effects. In another experiment, pituitary, but not hypothalamic, receptor was translocated to the nuclear fraction with an injection of 100 micrograms clomiphere (Clomid). Under these conditions serum LH is depressed, thus strengthening the hypothesis that, in the rat, estrogen action on the pituitary can cause suppression of serum LH independently of the hormone's action in the hypothalamus.

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Positive Feedback Sites of Estrogen in the Brain on Ovulation

Cited by 33 publications

References 8 publications

Localization and Mechanism of Stimulatory Feedback Action of Estrogen: Effect of Limbic Forebrain Implantation of Estradiol Benzoate on Advancement of Ovulation

Localization and Mechanism of Stimulatory Feedback Action of Estrogen: Effect of Limbic Forebrain Implantation of Estradiol Benzoate on Advancement of Ovulation

Study on the Bed Nucleus of Stria Terminalis in Relation to Gonadotropin Control

Differential sensitivity of estrogen target tissues: Implications for estrogen regulation of serum luteinizing hormone

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