scholarly journals Progesterone Priming Is Essential for the Full Expression of the Positive Feedback Effect of Estradiol in Inducing the Preovulatory Gonadotropin-Releasing Hormone Surge in the Ewe

Endocrinology ◽  
1999 ◽  
Vol 140 (1) ◽  
pp. 165-170 ◽  
Author(s):  
Alain Caraty ◽  
Donal C. Skinner

Abstract The luteal phase elevation in circulating progesterone (P) powerfully inhibits GnRH and, consequently, LH release, thereby preventing premature preovulatory LH surges in the ewe. Whether luteal phase P modulates the response of the GnRH system to the positive feedback effect of estradiol is unknown. To investigate this possibility, two experiments were conducted during the anestrous season using an artificial model of the follicular phase in ovariectomized ewes bearing 10-mm sc 17β-estradiol SILASTIC brand implants (Dow Corning Corp.). In Exp 1, ewes (n = 10) were run through four successive artificial cycles during which a luteal phase level of P was either replaced (cycles 1 and 3) or not replaced (cycles 2 and 4). GnRH and LH secretions were monitored by sampling cerebrospinal fluid (CSF) and jugular blood from 10–35 h after four 30-mm 17β-estradiol SILASTIC implants were inserted sc. CSF could be collected from only four ewes over the four cycles. There was no P-dependent difference in the onset of the GnRH and LH surges, which may have been due to a progressive delay in the surge onsets over the four cycles (by ANOVA, P < 0.05). Due to this delay, it was not possible to obtain an accurate estimate of the duration of the GnRH and LH surges in all ewes, but the size of the GnRH surge was always greater when animals had been treated with P, resulting in a significant increase in the maximum (P < 0.01) and mean (P < 0.05) levels during the surge. In contrast, there was no effect on any parameter of LH secretion. In Exp 2, ewes (n = 10) were run through two artificial estrous cycles during which luteal phase P was either replaced or not replaced, using a cross-over experimental design. CSF was collected from seven ewes over the two cycles. GnRH and LH secretions were monitored from 10–53 h after estradiol administration. As in Exp 1, a clear significant increase in the maximal and mean GnRH levels (P < 0.05 for both) was observed during the surge when ewes had been pretreated with P. Again, no changes were observed in LH release during the surge. P priming did, however, delay the onsets of the GnRH (P < 0.01) and LH surges (P < 0.01). Our data show that the increase in P during the luteal phase of the estrous cycle is essential for the full expression of the positive feedback effect of estradiol in inducing the preovulatory GnRH surge in the ewe.

1987 ◽  
Vol 115 (1) ◽  
pp. 16-20
Author(s):  
María R. Faigón ◽  
Berta Szwarcfarb ◽  
Pablo Scacchi ◽  
Jaime A. Moguilevsky

Abstract. The purpose of this study was to examine the role of opiate peptides in the development of the positive feedback effect of ovarian hormones (Oe-P) on the LH secretion that matures in female rats at about the age of 20–22 days. Oe-P administration at the age of 14 days induced a significant decrease of LH levels. A single injection of naloxone (5 mg/kg) induced a significant release of LH. This release was completely blocked by Oe-P administration. At the age of 20 days, Oe-P did not induce any significant change of LH levels, whereas naloxone increased the serum LH concentration. On the other hand, injection of Oe-P into naloxone-treated rats induced a significant rise in LH that was significantly higher than that observed with naloxone alone (P <0.025). Oe-P administration induced a positive feedback effect on LH at the age of 25 days. At this age, naloxone also increased LH levels and a significant potentiation of the LH release in response to Oe-P was observed in a group treated with naloxone. These results indicate that naloxone advances the development of the positive feedback mechanism of ovarian hormones on LH secretion and potentiates this mechanism after its maturation. On this basis it is proposed that the probable inhibitory effect of opiates on the onset of the positive feedback mechanism is related to the well-known participation of the opiate system in the onset of puberty. The LH release in response to naloxone significantly decreased from day 14 to day 25 and this could represent a decrease in the inhibitory effect of opiate peptides on LH secretion, probably connected with the onset of the postive feedback mechanism.


1970 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
S. TALEISNIK ◽  
M. E. VELASCO ◽  
J. J. ASTRADA

SUMMARY The influence that the interruption of the neural afferents to the hypothalamus exerts on ovulation and on the release of luteinizing hormone (LH) was studied in the rat. Animals with retrochiasmatic sections interrupting the neural connexions between the medial hypothalamus and the preoptic area (POA) showed constant oestrus and failed to ovulate. Animals in which the dorsal neural afferents to the POA were transected had oestrous cycles and ovulated normally. The positive feedback effect of progesterone on LH release in spayed animals primed either with 20 μg. oestradiol benzoate or 2·5 mg. testosterone propionate 3 days before was studied. Transection of the dorsal afferents to the POA favoured an increase in plasma LH, but in animals with retrochiasmatic sections the response was abolished. However, the negative feedback effect of ovarian steroids operated after both types of transection because an increase in plasma LH occurred after ovariectomy. It is concluded that the negative feedback effect of ovarian steroids acts on the medial hypothalamus which can maintain a tonic release of gonadotrophins in the absence of steroids. In contrast, the POA involved in the positive feedback effect of progesterone is concerned with the phasic release of LH.


1980 ◽  
Vol 33 (4) ◽  
pp. 465 ◽  
Author(s):  
PJ Wright ◽  
T Stelmasiak ◽  
WA Chamley

Oestradiol-17 p (40 fig intravenously) failed to elicit a surge in plasma LH levels by 13 h after administration in 64 % (16 out of 25) Merino ewes about 30 days post partum in the anoestrous season. LH-RH responsiveness and LH-RH priming effect were significantly greater in these ewes than in similar post-partum (n = 9) and non-parturient ewes (n = 3) not treated with oestradiol. This suggests that the failure of the oestrogen-positive feedback effect on LH release in post-partum ewes is not due to a failure of oestradiol action on the pituitary increasing pituitary responsiveness to LH-RH and LH-RH priming effect, but could be due to inadequate release of LH-RH from the hypothalamus.


1982 ◽  
Vol 100 (4) ◽  
pp. 492-498 ◽  
Author(s):  
Koji Koike ◽  
Toshihiro Aono ◽  
Hirohisa Tsutsumi ◽  
Akira Miyake ◽  
Keiichi Kurachi

Abstract. The effect of hyperprolactinaemia on the hypothalamo-pituitary axis was assessed by iv injection of 100 μg luteinizing hormone releasing hormone (LRH) in 7 women with prolactinoma before and 3 months after normalization of the Prl level by transsphenoidal surgery. A dose of 20 mg of conjugated oestrogen (Premarin®) was also injected iv into patients with prolactinoma before and 4 months after surgery, and the serum LH levels were determined serially for 120 h after the injection. Surgical treatment caused significant reduction of the mean (± se) serum prolactin (Prl) level from 123.3 ± 7.8 to 19.4 ± 5.6 ng/ml. But the differences in the basal levels of LH (11.3 ± 2.2 to 8.6 ± 1.5 mIU/ml), FSH (8.3 ± 2.4 to 10.6 ± 3.7 mIU/ml) and oestradiol (26.6 ± 8.6 to 37.5 ± 5.5 pg/ml) before and 4 months after surgery were not significant. An exaggerated LH response to LRH in untreated prolactinoma patients was also observed after surgical treatment. After surgical treatment, patients showed LH release with a peak between 48 and 72 h after the injection of Premarin, whereas before treatment they did not show any LH discharge. The mean percent increase in LH between 48 and 72 h was also significantly higher after operation than before operation. These results suggest that the hyperprolactinaemia in prolactinoma patients may cause an impaired positive feedback effect of oestrogen on LH release and that this derangement can be reversed by reduction of the Prl level by adenomectomy.


Endocrinology ◽  
2009 ◽  
Vol 150 (9) ◽  
pp. 4213-4220 ◽  
Author(s):  
Javed Iqbal ◽  
Olivier Latchoumanin ◽  
Ika P. Sari ◽  
Richard J. Lang ◽  
Harold A. Coleman ◽  
...  

Abstract In pituitary gonadotropes, estrogens have biphasic actions to cause an initial negative feedback followed by a positive feedback on LH secretion, but the mechanisms involved are not clearly understood. To investigate the feedback effects of estrogen, we used mixed ovine pituitary cell cultures (48–72 h), which were treated with 10−9m estradiol-17β (E2) or vehicle followed by a pulse of 10−9m GnRH. Medium was collected for LH assay and cells extracted to determine activation of MAPK (phosphorylated ERK-1/2). E2 treatment for 5 min reduced GnRH-induced LH release and caused phosphorylation of ERK-1/2. E2 alone also caused phosphorylation of ERK-1/2, similar to the response evoked by GnRH alone. GnRH increased cytoplasmic intracellular free calcium concentration ([Ca2+]i) and this was abolished by 2 min pretreatment with E2 or E-bovine serum albumen conjugate. Blockade of Ca2+ channels with nifedipine had no effect on the initial peak of GnRH-induced increase in [Ca2+]i but reduced its duration by 27 ± 6%. Depletion of intracellular Ca2+ stores with thapsigargin prevented GnRH-induced increase in [Ca2+]i. Thapsigargin (10−7m) or nifedipine (10−5m) pretreatment (15 min) of cells lowered GnRH-induced LH secretion by 30 ± 6 and 50% ± 4%, respectively. We conclude that inhibition of the GnRH-induced increase in [Ca2+]i in gonadotropes by E2 is a likely mechanism for the negative feedback effect of E2 on LH secretion involving a rapid nongenomic effect of E2. Activation of the MAPK pathway by E2 may be the mechanism for the time-delayed positive feedback effect on LH secretion at the level of the gonadotrope.


1981 ◽  
Vol 36 (6) ◽  
pp. 309-310
Author(s):  
El TERASAWA ◽  
JORGE F. RODRIGUEZ-SIERRA ◽  
DONALD J. DIERSCHKE ◽  
WILLIAM E. BRIDSON ◽  
ROBERT W. GOY

Andrologia ◽  
2012 ◽  
Vol 44 (4) ◽  
pp. 217-225 ◽  
Author(s):  
A. Kumar ◽  
R. Dewan ◽  
J. Suri ◽  
S. Kohli ◽  
S. Shekhar ◽  
...  

1980 ◽  
Vol 86 (3) ◽  
pp. 459-464 ◽  
Author(s):  
P. J. SHARP ◽  
R. MASSA

In the laying hen, progesterone was shown to be converted in vitro in the pituitary gland and the hypothalamus to 5β-pregnane-3,20-dione (5β-DHP), 5β-pregnan-3α-ol-20-one (5β,3α-ol) and 5α-pregnane-3,20-dione (5α-DHP) and in the hyperstriatum dorsale to 5β-DHP and 5β,3α-ol. The conversion of progesterone to 5β-reduced metabolites was greater in the hyperstriatum dorsale than in the hypothalamus (P<0·001) and greater in the hypothalamus than in the pituitary gland (P <0·01). The conversion of progesterone to 5β-reduced metabolites was greater than its conversion to 5α-DHP in the pituitary gland (P <0·01) and the hypothalamus (P < 0·001). The possibility was investigated that 5α-DHP and 5β-DHP may act as metabolic intermediaries in the mechanism by which progesterone exerts a positive feedback effect on LH release. Progesterone, 5α-DHP and 5β-DHP were injected into laying hens at doses of 0·05,0·25 and 1·25 mg/kg and the changes in the concentration of plasma LH were followed for 4 h thereafter. Secretion of LH was stimulated after treatment with progesterone or 5α-DHP but not 5β-DHP. Progesterone stimulated LH release more effectively than did 5α-DHP, since an increase in the concentration of plasma LH was observed after 0·25 mg progesterone/kg but not after the same dose of 5α-DHP. It was concluded that in the hen 5α-DHP is unlikely to play a role in the induction of the preovulatory release of LH.


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