LUTEINIZING HORMONE RELEASING FACTOR IN PITUITARY STALK PLASMA FROM LONG-TERM OVARIECTOMIZED RATS: EFFECTS OF STEROIDS

1980 ◽  
Vol 86 (3) ◽  
pp. 511-524 ◽  
Author(s):  
D. K. SARKAR ◽  
G. FINK
Keyword(s):  
Anterior Pituitary ◽  
Pituitary Stalk ◽  
Ovariectomized Rats ◽  
Circadian Pattern ◽  
Diurnal Pattern ◽  
Peripheral Plasma ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Venous Plasma

The concentration of LH releasing factor (LH-RF) was measured by radioimmunoassay in blood collected from the cut pituitary stalk of long-term ovariectomized rats anaesthetized with Althesin. Stalk plasma LH-RF concentrations were increased immediately after ovariectomy (carried out at oestrus) and low at 2 and 4 days after operation. The concentrations then began to increase to reach a level at 24–28 days which was significantly higher than the concentrations during the oestrous cycle except for the time of the ovulatory surge at pro-oestrus. This pattern was similar to that of the concentrations of LH in jugular venous plasma taken from the same animals before exposure of the pituitary stalk. Like peripheral plasma LH concentrations, the concentrations of LH-RF in stalk plasma fluctuated and fell significantly and rapidly after the intravenous injection of 1 μg oestradiol-17β. The release of LH-RF in long-term ovariectomized rats, into which had been implanted an oestradiol-containing Silastic capsule, was similar to the diurnal pattern of LH release; the afternoon increase in stalk plasma LH-RF concentration could be blocked by sodium pentobarbitone administered at 13.00 h and augmented by administering this anaesthetic at 13.00 h of the preceding day. The stalk plasma LH-RF concentrations in animals injec[unk]d with oestradiol benzoate (OB) followed 72 h later with either OB or progesterone were lower than the concentrations in animals injected only with oil. These data show that in the rat (1) ovarian steroids could moderate LH release ('negative feedback') by inhibiting LH-RF release, and that in long-term ovariectomized animals (2) the oestradiol-induced circadian pattern of LH release is due to a circadian pattern of LH-RF release, and (3) the surge of LH produced by administering OB followed by either OB or progesterone is probably due mainly to a massive increase in the responsiveness of the anterior pituitary gland to LH-RF.

Antioestrogen inhibition of oestradiol-induced alterations in hypothalamic noradrenaline turnover

1985 ◽  
Vol 106 (1) ◽  
pp. 37-42 ◽  
Author(s):  
C. Hiemke ◽  
B. Poetz ◽  
R. Ghraf
Keyword(s):  
Brain Area ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Noradrenaline Turnover ◽  
Stimulatory Action ◽  
Enhanced Sensitivity ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Secretory System

ABSTRACT Long-term (4–6 weeks) ovariectomized rats were injected with either oestradiol benzoate (OB; 20 μg s.c.) or monohydroxytamoxifen (MTAM; 0·2 mg i.p.) plus OB. Oestradiol benzoate was administered at 12.00 h on day 0 and MTAM was given immediately before OB, followed by further injections twice daily to maintain sufficiently high antioestrogen levels. When given alone, OB reduced the serum levels of LH during the morning (08.00–09.00 h) and afternoon (17.30–18.30 h) hours of day 3 after priming. The feedback actions of OB on LH release were accompanied by time-dependent alterations of noradrenaline turnover in the preoptic–anterior hypothalamic brain area (POAH). On day 3 after priming the noradrenaline turnover rate was reduced in the morning and increased in the afternoon. The increase correlated with an enhanced sensitivity of the LH secretory system to progesterone. The antioestrogen MTAM blocked the OB-induced sensitization of LH release to the stimulatory action of progesterone and interfered with the stimulatory long-term effect of oestradiol on hypothalamic noradrenaline turnover. The data strongly support the view that the oestrogen-induced afternoon increase of noradrenaline turnover in the POAH represents a pre-requisite for the induction of LH surges. The stimulatory effect of oestradiol on hypothalamic noradrenaline turnover seems to be mediated by a classical oestrogen receptor mechanism. J. Endocr. (1985) 106, 37–42

RESTORATION BY OESTRADIOL BENZOATE OF A NEURAL AND HORMONAL RHYTHM IN THE OVARIECTOMIZED RAT

1975 ◽  
Vol 64 (1) ◽  
pp. 27-35 ◽  
Author(s):  
F. R. BURNET ◽  
P. C. B. MACKINNON
Keyword(s):  
Single Injection ◽  
Time Of Day ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Functional Link ◽  
Initial Injection ◽  
Oestradiol Benzoate ◽  
Before And After ◽  
Lh Release ◽  
The Brain

SUMMARY The rate of [35S]methionine incorporation into protein in discrete cerebral areas was measured before and after the administration of oestradiol benzoate (OB) to chronically ovariectomized rats. The circadian rhythm of incorporation which is normally seen in the intact cyclic female rat was deleted by ovariectomy. A daily rhythm of incorporation reappeared, however, in all the brain areas studied 30 h after a single injection of OB (20 μg), and was still present 12 days later. The release of luteinizing hormone (LH) after administration of 20 μg OB was measured in chronically ovariectomized animals and was found to be biphasic. High levels of LH after ovariectomy were initially reduced by negative feedback, but this phase was followed 52 h later by a facilitation of LH release between 15.00 and 18.00 h. The facilitation of LH release at this time of day was still detectable 12 days after the initial injection. The evidence for a functional link between the rhythm of neural activity which is reflected by [35S]methionine incorporation, and the ability to 'time' the facilitation of LH release is discussed.

Influence of melatonin and oestradiol on the opioidergic regulation of LH and prolactin release in pony mares

1997 ◽  
Vol 154 (2) ◽  
pp. 241-248 ◽  
Author(s):  
C Aurich ◽  
J Lange ◽  
H-O Hoppen ◽  
J E Aurich
Keyword(s):  
Prolactin Secretion ◽  
Opioid Antagonist ◽  
Short Term ◽  
Melatonin Treatment ◽  
Prolactin Release ◽  
Oestradiol Treatment ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

Abstract The aim of this study was to investigate the influence of oestradiol, melatonin and season on the opioid regulation of LH and prolactin release. Effects of the opioid antagonist naloxone (0·5 mg/kg) on LH and prolactin secretion were determined in ovariectomized pony mares. In experiment 1, mares in January (n=6) were pretreated with oestradiol benzoate (5 μg/kg) for 20 days. In experiment 2, beginning in May, mares (n=7) received melatonin (15 mg) for 15 days and subsequently a combination of melatonin plus oestradiol for 20 days. In experiment 3, beginning in May, mares (n=6) were pretreated with oestradiol for 30 days, left untreated for 12 days and then given melatonin for 35 days. In all experiments the animals were injected with the opioid antagonist naloxone and saline on 2 consecutive days prior to treatment. In experiment 1, animals received naloxone and saline on days 10 and 11 and 20 and 21 following oestradiol treatment. In experiment 2, naloxone and saline were administered on days 15 and 16 following melatonin treatment and on days 10 and 11 and 20 and 21 of melatonin plus oestradiol treatment. In experiment 3, the animals received naloxone and saline on days 10 and 11, 20 and 21 and 30 and 31 of oestradiol treatment, prior to melatonin treatment and on days 15 and 16, 25 and 26 and 35 and 36 following melatonin. In January (experiment 1), naloxone evoked a significant (P<0·05) LH release at all times, however the LH increment in response to naloxone increased during oestradiol pretreatment (P<0·05) During the breeding season (experiments 2 and 3), naloxone induced a significant (P<0·05) increase in plasma LH concentrations when mares had not been pretreated with oestradiol or melatonin and after oestradiol pretreatment. Basal LH concentrations and the LH increment in response to naloxone increased significantly (P<0·05) during the 30-day oestradiol pretreatment. Melatonin decreased the naloxone-induced LH release and the LH release in response to naloxone and saline no longer differed after 25 and 35 days of melatonin pretreatment. When melatonin was given together with oestradiol for 20 days, again a significant (P<0·05) LH release in response to naloxone occurred. Prolactin release was significantly (P<0·05) increased by naloxone when mares had been pretreated with only melatonin. The opioid antagonist did not affect prolactin release in mares that had not been pretreated or received oestradiol either alone or in combination with melatonin. In conclusion, in long-term ovariectomized mares, opioids inhibit LH secretion independent from ovarian factors. This opioid inhibition of LH secretion is enhanced by oestradiol and reduced by melatonin. Although short-term melatonin treatment in-activates the opioid regulation of LH release, a prolonged influence of melatonin as occurs in winter does not prevent activation of the opioid system. This indicates that effects of melatonin on the opioid regulation of LH release change with time. An opioid inhibition of prolactin secretion is activated by melatonin given for 15–35 days but is lost under the prolonged influence of a short-day melatonin signal in winter. Journal of Endocrinology (1997) 154, 241–248

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

Inhibition of phasic but not tonic pituitary secretion by 2-hydroxyoestrone in the rat: evidence of action as an oestrogen antagonist

1983 ◽  
Vol 98 (1) ◽  
pp. 103-112 ◽  
Author(s):  
Shigehiro Katayama ◽  
Jack Fishman
Keyword(s):  
Pituitary Hormones ◽  
Ovariectomized Rats ◽  
Priming Dose ◽  
Physiological Mechanisms ◽  
Lh Surge ◽  
Oestradiol Benzoate ◽  
Pituitary Secretion ◽  
The Brain ◽  
Phasic Release

Rats with 4-day oestrous cycles, implanted with intracardiac catheters, were injected with 2-hydroxyoestrone at noon on pro-oestrus and their plasma LH levels monitored at frequent intervals thereafter. A dose of 100 μg 2-hydroxyoestrone completely abolished the preovulatory LH rise in four out of ten animals tested, showing no effect in the six others. When an injection of 10 μg oestradiol 1 h before the 2-hydroxyoestrone administration was given all the rats showed an absence of the preovulatory LH surge, while it remained intact in the controls treated with oestradiol only. The principal metabolite of 2-hydroxyoestrone, 2-methoxyoestrone, exhibited no influence on the pituitary gonadotrophin release. Repeated injections of 100 pg doses of 2-hydroxyoestrone to long-term ovariectomized rats produced no change in plasma LH and prolactin levels. In animals primed with oestradiol benzoate, 2-hydroxyoestrone given 1–2 h after the priming dose blocked the phasic release of the pituitary hormones on the afternoon of the 2 subsequent days. The LH and prolactin surges in the primed animals, however, were not affected when the catechol oestrogen was injected 2 h before their appearance. These results indicate that in the cyclic rat exogenous 2-hydroxyoestrone inhibits the preovulatory LH surge when its administration is coincident with the preovulatory oestradiol rise. In the ovariectomized rat 2-hydroxyoestrone inhibits the oestrogen-dependent priming step but does not affect either the oestrogen-independent expression of the induced surges or the tonic secretion of these pituitary hormones. These results indicate a dissociation of central and peripheral activities in this oestradiol metabolite and suggest that this catechol oestrogen functions as an oestrogen antagonist in neuroendocrine events. Since catechol oestrogens can be formed in the brain these pharmacological responses may reflect physiological mechanisms.

Dissociation between the ovarian factors controlling sexual receptivity and preovulatory secretion of LH in cyclic female rats

1987 ◽  
Vol 112 (1) ◽  
pp. 133-138 ◽  
Author(s):  
P. Södersten ◽  
P. Eneroth
Keyword(s):  
Sexual Behaviour ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Serum Progesterone ◽  
Lh Surge ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion ◽  
Intact Rats

ABSTRACT Ovariectomy and treatment with oestradiol benzoate (10 μg OB) on the day before behavioural oestrus eliminated the preovulatory surge of LH and reduced the level of sexual receptivity on the following day. Sexual behaviour, but not the LH surge, was restored by progesterone (0·5 mg) given 18 h later. Injection of OB on the day after behavioural oestrus induced a small release of LH and normal sexual behaviour on the following day. Ovariectomy on the day after behavioural oestrus reduced the stimulatory effect of OB on sexual behaviour and eliminated its weakly stimulatory effect on LH release. Sexual behaviour, but not the small LH surge, was restored in these animals by progesterone (0·5 mg) given 18 h later. Treatment of rats ovariectomized 2 days before the day of the LH surge with implants containing oestradiol or injections of oestradiol (1 μg) induced LH surges but the amplitudes of these LH surges were much smaller than those of the normal LH surge. Treatment of intact rats with OB increased serum progesterone levels 24 h later, an effect which was eliminated by ovariectomy. Injections of LH (20 μg) into intact rats on the day after behavioural oestrus also increased serum progesterone concentrations but failed to stimulate sexual behaviour. It is suggested that OB treatment of intact rats on the day after behavioural oestrus stimulates sexual behaviour by inducing a surge of LH secretion which activates ovarian secretion of progesterone. Thus, oestrogen and progesterone but not the LH surge are essential for sexual behaviour. Whereas oestradiol and progesterone restore normal sexual behaviour in ovariectomized rats, additional ovarian factors may be required for induction of normal LH surges. J. Endocr. (1987) 112, 133–138

scholarly journals Oestrogens regulate pituitary alpha2,3-sialyltransferase messenger ribonucleic acid levels in the female rat

1999 ◽  
Vol 23 (2) ◽  
pp. 153-165 ◽  
Author(s):  
P Damian-Matsumura ◽  
V Zaga ◽  
A Maldonado ◽  
C Sanchez-Hernandez ◽  
C Timossi ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Cdna Probe ◽  
Ovariectomized Rats ◽  
Molecular Forms ◽  
Northern Blot Hybridization ◽  
Mrna Levels ◽  
Female Rat ◽  
Messenger Ribonucleic Acid ◽  
Ici 182,780 ◽  
Oestradiol Benzoate

Follicle-stimulating hormone (FSH) is synthesized by the anterior pituitary gland in multiple molecular forms. Increased acidic/sialylated FSH charge isoforms are associated with conditions characterized by a low oestrogen output. In the present study, we analysed the dynamics of the changes in mRNA levels of the enzyme Galbeta1,3[4]GlcNAc alpha2,3-sialyltransferase (2,3-STase) (one of the enzymes that incorporate sialic acid residues into the FSH molecule) in intact and ovariectomized rats. The anterior pituitaries of 4-day regularly cyclic adult female Wistar rats were obtained at 1000 h on the days of pro-oestrus (P), oestrus (O), dioestrus 1 (D1) and dioestrus 2 (D2), at 0200 h, 1400 h, 1800 h and 2200 h on D1, at 1800 h on day of O and at 1000 h after 7, 14, 21, 28 and 45 days of oophorectomy performed on the morning of P. Total RNA was isolated from each gland and the 2,3-STase levels were measured by Northern blot hybridization analysis employing a 346-base pair cDNA probe encoding for a non-conserved amino acid sequence of the catalytic domain of the enzyme. Maximal levels of the enzyme mRNA were detected at 1000 h on D1; thereafter, they progressively decreased by 60% during the ensuing 24 h, reaching the lowest concentration values (26% of the maximally observed level on D1) at 1000 h on day of P and remaining unchanged during the morning of O. Administration of the potent oestradiol receptor antagonist ICI 182,780 at 1000 h on D1 completely reverted the time-dependent decrease in 2,3-STase mRNA levels observed during the afternoon of D1, whereas oestradiol benzoate administered at 1000 h on day of O significantly reduced the enzyme mRNA levels (to 21% of the levels detected in vehicle-treated controls). In ovariectomized rats, the alpha2,3-STase mRNA progressively increased from day 21 to day 45 post castration. Administration of oestradiol benzoate on day 28 after oophorectomy significantly reduced the 2,3-STase mRNA levels (to 36% of the levels detected in vehicle-injected controls); ICI 182,780 partially counteracted this oestradiol-mediated effect. The dynamics of these changes in 2,3-STase mRNA levels partially correlated with changes in the relative abundance of the FSH charge isoforms separated by preparative chromatofocusing of anterior pituitary extracts, particularly in glands obtained during the morning of P and O. These data demonstrate for the first time that pituitary 2,3-STase is a hormonally-regulated enzyme and that the changes in transcription and/or stability of its mRNA may be involved, in part, in the post-translational processing of the FSH molecule during certain physiological conditions.

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro

1981 ◽  
Vol 240 (2) ◽  
pp. E125-E130 ◽  
Author(s):  
E. Y. Adashi ◽  
A. J. Hsueh ◽  
T. H. Bambino ◽  
S. S. Yen
Keyword(s):  
Anterior Pituitary ◽  
Clomiphene Citrate ◽  
Follicle Stimulating Hormone ◽  
Significant Inhibition ◽  
Ovariectomized Rats ◽  
Pituitary Cells ◽  
Direct Effects ◽  
Lh Release ◽  
Sensitizing Effect

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.

Effects of oestradiol benzoate and progesterone on luteinizing hormone release and catecholamine turnover in the preoptic-hypothalamic brain area of ovariectomized rats

1983 ◽  
Vol 97 (3) ◽  
pp. 437-445 ◽  
Author(s):  
C. Hiemke ◽  
D. Frohne ◽  
D. Bruder ◽  
R. Ghraf
Keyword(s):  
Brain Area ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Time Interval ◽  
Dopamine Turnover ◽  
Noradrenaline Turnover ◽  
Serum Lh ◽  
Short Term Exposure ◽  
Oestradiol Benzoate

At noon, long-term (4–6 weeks) ovariectomized rats were exposed for 6–78 h to a single subcutaneous injection of oestradiol benzoate (20 μg) which significantly reduced the serum levels of LH over the whole time-interval investigated. The negative feedback action of oestradiol was accompanied by reduced turnover of both noradrenaline and dopamine in the preoptic-anterior hypothalamic brain area (POAH), but not in the mediobasal hypothalamus, 6, 68 and 72 h after administration of the hormone. Between 72 and 78 h after oestradiol-priming an afternoon increase of noradrenaline turnover was observed in the POAH. In rats primed with oestradiol benzoate for 72 h, short-term exposure (6 h) to progesterone (2·5 mg) induced a marked surge of serum LH and FSH in the late afternoon. In the POAH of these rats progesterone did not interfere with the afternoon increase of noradrenaline turnover induced by oestradiol-priming. However, it markedly increased the dopamine turnover rate of primed rats, thus reversing the inhibitory action of oestradiol benzoate on the dopaminergic system of the POAH. It is concluded that both the noradrenergic and the dopaminergic neurones of the POAH are involved in the negative and positive feedback actions of oestradiol and progesterone on LH and FSH release. The paper discusses whether the oestradiol-induced afternoon increase in noradrenaline turnover represents a prerequisite for the induction of LH surges by progesterone.

A possible role of clomiphene citrate in the control of pre-ovulatory LH surge during induction of ovulation

1985 ◽  
Vol 109 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Naoki Terakawa ◽  
Ikuya Shimizu ◽  
Hirohisa Tsutsumi ◽  
Toshihiro Aono ◽  
Keishi Matsumoto
Keyword(s):  
Nuclear Receptor ◽  
Clomiphene Citrate ◽  
Ovariectomized Rats ◽  
Receptor Complex ◽  
Oestrogen Receptors ◽  
Lh Surge ◽  
Serum Lh ◽  
Lh Release

Abstract. A possible role of clomiphene citrate (clomiphene) in the control of ovulation in anovulatory women was investigated. Since a single ip administration of 5 μg oestradiol-17β (E2) to long-term ovariectomized rats did not induce LH surge, the following studies were designed to determine whether pretreatment with clomiphene followed by administration of E2 could induce LH surge in the ovariectomized rats. Changes in cytoplasmic and nuclear oestrogen receptors (ER) were also examined in the pituitaries of these animals. An ip injection of 200 μg clomiphene suppressed serum LH levels significantly for 72 h. The clomiphene injection rapidly caused an elevation of nuclear ER with a concomitant depletion of cytoplasmic ER level in the pituitary and the ER levels remained almost unchaged for 72 h. An administration of E2 12 or 24 h after the clomiphene injection had no significant effects on either the serum LH levels or the cytoplasmic and nuclear ER levels, compared with those induced by clomiphene alone. However, LH surge and the depletion of nuclear ER in the pituitary occurred 24 h later when E2 was injected 48 h after the clomiphene administration. The E2-induced LH release seems to be induced by a replacement of clomiphene by E2 on the nuclear receptor complex. These results suggest that clomiphene may exert actions directly on the pituitary gland to augment oestrogeninduced LH release.

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