Interaction of the anti-estrogen CI-628 and estradiol on plasma LH and hypothalamic LH-RH in the female rat

Gogan, F.; Rotsztejn, W.H.; Couturier, Laurence; Chazal, Geneviève; Beattie, I A; Kordon, C.

doi:10.1016/0006-8993(80)90590-9

Cited by 18 publications

(12 citation statements)

References 39 publications

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“…LH secretory surges observed in OVX-E2 ani mals [3,13,15,17,32] can be either amplified or inhibited by progesterone, depending upon the timing of progeste rone pretreatment. A 4-hour time interval between hormone administration and the expected LH surge markedly in creased LH secretion, whereas a 16-to 36-hour time interval completely blocked the LH surge.…”

Section: Discussionmentioning

confidence: 99%

“…Three groups of animals were studied: (a) OVX rats: (b) OVX-E: rats, i.e. OVX rats implanted subcutaneous ly for 5 days with 0.5-cm-long Silastic implants containing 8 mg of 17|)-estradiol (E. Merck), a treatment previously shown to elicit steady-state E: plasma levels in the range of 41 ± 3 pg/ml in OVX animals [17]; (c) OVX-E, rats treated with progesterone (25 mg/rat [16,31], Lutogyl, Roussel)4, 16or36h prior to the experiment.…”

Section: Methodsmentioning

confidence: 99%

“…Blood sampling (400 pi per sample) was achieved through the polyethylene cannula, at 09.00, 11.00, 13.00, 15.00, 17.00, and 19.00 h in unanesthetized, unrestrained rats. Plasma samples were analyzed for LH by a specific double-antibody radioimmunoassay [13,17]. LH values are expressed as nanograms per milliliter of NIAMDDrat LH RPI.…”

Section: Methodsmentioning

confidence: 99%

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Effects of Ovarian Steroids on in vitro Release of LHRH from Mediobasal Hypothalamus

Drouva

Laplante

Kordon³

1983

Neuroendocrinology

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The phasic luteinizing hormone (LH) release observed in ovariectomized (OVX), estrogen-implanted rats was further amplified and advanced when progesterone (P) was given 4 h prior to the gonadotropin surge. In contrast, an inhibitory effect of P on the daily LH surge was observed when P was administered 16–36 h prior to LH peak. In order to determine whether this biphasic action of P is primarily exerted on the release of luteinizing hormone releasing hormone (LHRH), on the pituitary response to LHRH, or on both, mediobasal hypothalamic slices or pituitary fragments of adult OVX rats or of OVX rats pretreated with estrogen alone or in combination with P were tested in a perifusion system. Mediobasal hypothalamic slices were perifused in buffered (pH 7.2) oxygenated Locke’s medium containing bacitracin (2 × 10^–5 M). In the absence of estrogen pretreatment, high (56 mM) concentrations of K⁺ were barely effective in releasing LHRH. Subcutaneous implantation of 17β-estradiol for 5 days markedly increased the amplitude of the LHRH secretory response to K⁺ depolarization. Additional administration of P (25 mg/rat s.c.) 4 h before sacrifice further amplified the K⁺-induced LHRH release. In contrast, the K⁺-evoked LHRH secretion was significantly inhibited when P was given 16 or 36 h before. Estradiol thus appears to facilitate the LHRH secretory response to depolarizing stimuli, whereas P either enhances or blocks the induced LHRH release depending upon its time of administration. At the pituitary level, the sensitivity of LHRH-induced LH release was also increased after estrogen pretreatment. P either enhanced the effect 4 h after its administration or completely inhibited it after 16 or 36 h. These results suggest that parallel interactions of the steroid at the level of both LHRH neurons and the pituitary may account for their in vivo effects.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Effects of Ovarian Steroids on in vitro Release of LHRH from Mediobasal Hypothalamus

Drouva

Laplante

Kordon³

1983

Neuroendocrinology

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“…Food and water were supplied ad libitum. 4 or 5 weeks after ovari ectomy, some of the animals were implanted subcutaneously for 5 days with 0.5 cm long Silastic capsules containing 8 mg of either 17|J-estradiol, a procedure shown to elicit steady-state plasma levels of the steroid in the range of 41 ± 3 pg/ml in OVX rats [22], I7a-estradiol, or stilbestrol. …”

mentioning

confidence: 99%

Effects of 17β-Estradiol on LH-RH Release from Rat Mediobasal Hypothalamic Slices

Drouva¹,

Laplante²,

Gautron³

et al. 1984

Neuroendocrinology

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Mediobasal hypothalamic slices of adult ovariectomized (OVX) rats treated or not with 17β-estradiol (E₂) were superfused in buffered (pH 7.2) Locke medium containing bacitracin. A 6-min pulse of K⁺ (56 m M) was less effective in releasing luteinizing hormone releasing hormone (LH-RH) from mediobasal hypothalamic slices sampled from OVX rats than from OVX animals treated subcutaneously with either E₂ or stilbestrol implants for 5 days; in contrast, the basal release of the neuropeptide was identical in both cases. Direct addition to the superfusion medium of 17β-estradiol (10^–10 to 10^–7M) or stilbestrol (10^–8M) potentiated the K⁺-induced LH-RH release from slices of OVX animals. The K⁺-induced LH-RH release observed after in vivo E₂ implantation was not further amplified by in vitro addition of the hormone. Tamoxifen and hydroxytamoxifen, estrogen antagonists, were ineffective by themselves, but reversed the E₂ facilitation of K⁺-evoked LH-RH release. In contrast, 17α-estradiol, progesterone, or cholesterol (10^–8 or 10^–9M) hat no effect on either basal or stimualted release of the neurohormone. Somatostatin release measured under identical conditions was not affected by castration or by in vitro addition of the steroid. In conclusion: (1) estradiol appears selectively and specifically involved in the process coupling, nerve endings depolarization, and LH-RH release, and (2) the effect is receptor-mediated and does not appear, to require nuclear translocation of the steroid or transcription processes, since it can be readily elicited upon addition of the hormone to nerve endings disconnected from their cell bodies.

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“…1 and 3, Tables 1 and 2) demonstrate that the inhibi tory effect of antiestrogen on the ovary is due to disappearance of the LH surge on the after noon of proestrus. Gogan et al (26) indicated that antiestrogen, nitromophene citrate, acted at the pituitary level to decrease its sensitivity to LH-RH rather than direct action on the hypothalamus in female rats. There are many reports that the pituitary is a site for the posi tive effect of steroids (27,28).…”

Section: Discussionmentioning

confidence: 99%

Effects of Antiestrogens on Ovarian Aldo-Keto Reductase in Relation to Ovulation in Rats.

Inaba¹,

Inazu²,

Kuroda³

et al. 1991

Jpn.J.Pharmacol

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Interaction of the anti-estrogen CI-628 and estradiol on plasma LH and hypothalamic LH-RH in the female rat

Cited by 18 publications

References 39 publications

Effects of Ovarian Steroids on in vitro Release of LHRH from Mediobasal Hypothalamus

Effects of Ovarian Steroids on in vitro Release of LHRH from Mediobasal Hypothalamus

Effects of 17β-Estradiol on LH-RH Release from Rat Mediobasal Hypothalamic Slices

Effects of Antiestrogens on Ovarian Aldo-Keto Reductase in Relation to Ovulation in Rats.

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