scholarly journals Ovarian stimulation with FSH reduces phosphorylation of gonadotrope progesterone receptor and LH secretion in the rat

Reproduction ◽  
2009 ◽  
Vol 137 (1) ◽  
pp. 151-159 ◽  
Author(s):  
Ana Gordon ◽  
José C Garrido-Gracia ◽  
Rafaela Aguilar ◽  
Silvia Guil-Luna ◽  
Yolanda Millán ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Ovarian Stimulation ◽  
Inhibitory Effect ◽  
Ovx Rats ◽  
Formalin Fixed Paraffin ◽  
Formalin Fixed Paraffin Embedded ◽  
Experimental Approaches ◽  
Lh Release ◽  
Lh Secretion

Administration of human FSH (hFSH) to cyclic rats during the dioestrous phase attenuates progesterone receptor (PR)-dependent events of the preovulatory LH surge in pro-oestrus. The increased bioactivity of the putative ovarian gonadotropin surge inhibiting/attenuating factor induced by hFSH treatment is not associated with a decrease in PR protein expression, and the possibility of its association at a PR posttranslational effect has been raised. The present experiments aimed to analyse PR phosphorylation status in the gonadotrope of rats with impaired LH secretion induced byin vivohFSH injection. Two experimental approaches were used. First, incubated pro-oestrous pituitaries from hFSH-injected cycling and oestrogen-treated ovariectomized (OVX) rats were used to analyze the effect of calyculin, an inhibitor of intracellular phosphatases, on PR-dependent LH release, which was measured in the incubation medium by RIA. Second, pituitaries taken from hFSH-injected intact cycling and OVX rats and later incubated with P or GNRH1 were used to assess the phosphorylation rate of gonadotrope. The latter was analysed in formalin-fixed, paraffin-embedded tissue sections by immunohistochemistry using a MAB that recognizes the phosphorylated (p) form of PR at Ser294. Calyculin reduced the ovary-mediated inhibition of hFSH in GNRH1-stimulated LH secretion. In addition, the immunohistochemical expression of pSer294 PR was significantly reduced after ovarian stimulation with hFSH in pituitaries from pro-oestrous rats incubated with P or GNRH1. Altogether, these results suggested that the ovarian-dependent inhibitory effect of FSH injection on the preovulatory LH secretion in the rat may involve an increase in dephosphorylation of PR.

scholarly journals Oestradiol-17β inhibits tamoxifen-induced LHRH self-priming blocking hormone-dependent and ligand-independent activation of the gonadotrope progesterone receptor in the rat

2006 ◽  
Vol 190 (1) ◽  
pp. 73-84 ◽  
Author(s):  
José E Sánchez-Criado ◽  
José C Garrido-Gracia ◽  
Carmina Bellido ◽  
Rafaela Aguilar ◽  
Pedro Guelmes ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Protein Phosphatases ◽  
Estrogen Receptor Α ◽  
Inhibitory Effect ◽  
Cellular Protein ◽  
Pituitary Cells ◽  
Camp Content ◽  
Agonist Action ◽  
Ovx Rats ◽  
Lh Secretion

In the rat, administration of tamoxifen (TX) in the absence of oestrogen (E) induces LHRH self-priming, the progesterone receptor (PR)-dependent property of LHRH that increases gonadotrope responsiveness to itself. The oestrogen-dependent PR can be phosphorylated/activated by progesterone (P4) and, in the absence of the cognate ligand, by intracellular LHRH signals, particularly cAMP/protein kinase A. We have recently found that oestradiol-17β (E2), acting on a putative membrane estrogen receptor-α in the gonadotrope, inhibits this agonist action of TX. This study investigated the mechanism by which E2 inhibits TX-elicited LHRH self-priming using both incubated pituitaries from TX-treated ovariectomized (OVX) rats and anterior pituitary cells from OVX rats cultured with TX. It was found that (1) in addition to the inhibitory effect on TX-elicited LHRH self-priming, E2 blocked P4 and adenylyl cyclase activator forskolin augmentation of LHRH-stimulated LH secretion, and (2) E2 did not affect the increasing action of TX on gonadotrope PR expression or pituitary cAMP content. Furthermore, inhibition of protein phosphatases with okadaic acid suppressed E2 inhibition of TX-elicited LHRH-induced LH secretion, while stimulation of protein phosphatases with ceramide blocked TX-induced LHRH self-priming. Together, these results indicated that membrane ER-mediated E2 inhibition of the TX-stimulated LHRH self-priming pathway involves a blockade of gonadotrope PR phosphorylation/activation, but not a deficient response of PR to phosphorylases. Results also suggested that the inhibitory effect of E2on TX-induced LHRH self-priming is exerted through modulation of cellular protein phosphatase activity in the gonadotrope.

scholarly journals Antiprogestins RU486 and ZK299 suppress basal and LHRH-stimulated FSH and LH secretion at pituitary level in the rat in an oestrous cycle stage-dependent manner

1999 ◽  
Vol 163 (1) ◽  
pp. 79-85 ◽  
Author(s):  
C Bellido ◽  
D Gonzalez ◽  
R Aguilar ◽  
JE Sanchez-Criado
Keyword(s):  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Type I ◽  
Dependent Manner ◽  
Natural Ligand ◽  
Ovx Rats ◽  
20 Nm ◽  
Lh Secretion

We have previously shown that administration of antiprogestin (AP) type II RU486 to ovariectomized (OVX) rats on the morning of pro-oestrus decreases the magnitude of preovulatory gonadotrophin surge. This suggests that the effect of RU486 on LHRH-dependent gonadotrophin release may be independent of its ability to block progesterone actions. The aim of the present research was to study the possible site of RU486 action and to determine whether the gonadotrophin suppressive effect of APs RU486 and ZK299 is dependent on the oestrogen background. Intact or OVX rats in the morning of pro-oestrus were injected s.c. with 4 mg of RU486 or ZK299 (AP type I) at 0900 h on pro-oestrus. At 1830 h, serum concentration of FSH and LH and median eminence (ME) content of LHRH were determined. In the second experiment, the effect of RU486 and ZK299 on pituitary responsiveness to LHRH (100 ng, i.p.) and ME content of LHRH at 1830 h pentobarbital-blocked intact or OVX rats was evaluated. In the last study, the anterior pituitary release of FSH and LH from pro-oestrus or metoestrus donors incubated with or without LHRH (1, 10 or 100 nM) in the presence or absence of APs (20 nM) was evaluated. Both APs reduced serum FSH and LH levels at 1830 h on pro-oestrus in intact and OVX rats. The suppressive effect on gonadotrophin release brought about by AP treatment was also evidenced in PB-blocked intact and OVX rats. This suggested that the inhibitory effect of APs occurred, at least in part, at pituitary level. Furthermore, in the absence of the natural ligand, APs significantly reduced basal and LHRH-stimulated FSH and LH release from pro-oestrous but not from metoestrus pituitaries. In conclusion, these experiments have shown, both 'in vivo' and 'in vitro', that APs RU486 and ZK299 have suppressive effects at pituitary level on basal and LHRH-stimulated FSH and LH secretion, regardless of their antiprogestagenic activity, in pro-oestrus but not in metoestrus.

scholarly journals Effects of non-steroidal gonadal factors on LH secretion in female common carp during the reproductive cycle

2008 ◽  
Vol 53 (No. 9) ◽  
pp. 398-403
Author(s):  
J. Chyb ◽  
T. Mikolajczyk ◽  
M. Sokolowska-Mikolajczyk ◽  
M. Socha ◽  
P. Szczerbik ◽  
...  
Keyword(s):  
Common Carp ◽  
Reproductive Cycle ◽  
Inhibitory Effect ◽  
Gonad Maturity ◽  
Lh Release ◽  
Gonadal Recrudescence ◽  
Lh Secretion

The aim of this study was to evaluate the effects of recombinant human inhibin A, recombinant human activin A and desteroidized ovarian extract on LH secretion <I>in vitro</I> and <I>in vivo</I> in female common carp during different stages of reproductive cycle. Inhibin stimulated spontaneous as well as GnRH-stimulated LH release <I>in vivo</I> in fish during gonadal recrudescence. This hormone did not have an influence on spontaneous LH secretion in the periovulatory period, but had a slightly inhibitory effect on GnRH-stimulated LH release in this stage of gonad maturity. Activin decreased spontaneous LH secretion during gonadal recrudescence and increased LH secretion before ovulation, having no effects on GnRH-stimulated LH release during both stages of gonad maturity. The desteroidized ovarian extract failed to modify spontaneous LH secretion, but decreased GnRH-stimulated LH release during recrudescence and especially before ovulation. It is to conclude that these data suggest the differential role of inhibin/activin as substances in the regulation of LH secretion in common carp females.

Kinetics of LRH-induced LH-release in vivo: influence of LRH pre-treatment

1982 ◽  
Vol 99 (2) ◽  
pp. 195-199 ◽  
Author(s):  
T. R. Koiter ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling
Keyword(s):  
Priming Effect ◽  
Compartment Model ◽  
Secretion Rate ◽  
Ovx Rats ◽  
Lh Release ◽  
The Mean ◽  
Pre Treatment ◽  
Lh Secretion ◽  
Secretion Rates

Abstract. The influence of an LRH injection (50 ng/ 100 g b.w.) on the LH-response to a second, equally large LRH injection or a constant rate infusion of LRH (104 ng/h), administered 1 h later, was studied in phenobarbitone-anaesthetized, oil- or oestradiol benzoate (OeB)-treated rats ovariectomized (OVX) 5 weeks earlier. From the plasma LH concentration the mean maximal LH secretion rates, as well as the amounts of LH secreted, were calculated on the basis of a one-compartment model, proceeding from a half-life of LH of 15 min. In both the oil- and the OeB-treated animals, not only the mean maximal LH secretion rate, but also the amount of LH secreted during the first hour following the injection, was significantly higher after the second LRH injection than after the first one (LRH self-priming effect). Infusion of LRH in LRH-primed OVX rats revealed that the LH secretion accelerates immediately after the start of the infusion and this acceleration lasts about 1 h. In the saline-injected controls, on the other hand, the LH secretion, although elevated, remains constant during the first 30 min of LRH infusion and accelerates only thereafter during about 1 h. Yet, maximal LH secretion rates are not statistically different between the LRH-primed oil- or OeB-treated OVX rats and their respective saline-injected controls. It is concluded that the self-priming effect of LRH does not lead to an increase of the ultimate maximal LH secretion rate. Rather, during priming the conditions necessary for immediate acceleration of the LH secretion rate are established, and priming thus causes a shift in time, that is, an advancement, of the LH-response to a subsequent LRH stimulus.

scholarly journals The integrated action of oestrogen receptor isoforms and sites with progesterone receptor in the gonadotrope modulates LH secretion: evidence from tamoxifen-treated ovariectomized rats

2007 ◽  
Vol 193 (1) ◽  
pp. 107-119 ◽  
Author(s):  
José C Garrido-Gracia ◽  
Ana Gordon ◽  
Carmina Bellido ◽  
Rafaela Aguilar ◽  
Inmaculada Barranco ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Oestrogen Receptor ◽  
Ovariectomized Rats ◽  
The Past ◽  
Receptor Isoforms ◽  
Ovx Rats ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Lh Secretion

The specific role of each oestrogen receptor (ER) isoform (α and β ) and site (nucleus and plasma membrane) in LH release was determined in ovariectomized (OVX) rats injected over 6 days (days 15–20 after OVX) with a saturating dose (3 mg/day) of tamoxifen (TX), a selective ER modulator with nuclear ERα agonist actions in the absence of oestrogen. This pharmacological effect of TX was demonstrated by the fact that it was blocked by the selective ERα antagonist methyl-piperidinopyrazole. Over the past 3 days of the 6-day TX treatment, rats received either 25 μg/day oestradiol benzoate (EB), 1.5 mg/day selective ERα agonist propylpyrazole triol (PPT) and the selective ERβ agonist diarylpropionitrile (DPN), or a single 3 mg injection of the antiprogestin onapristone (ZK299) administered on day 20. Blood samples were taken to determine basal and progesterone receptor (PR)-dependent LH-releasing hormone (LHRH)-stimulated LH secretion and to evaluate LHRH self-priming, the property of LHRH that increases gonadotrope responsiveness to itself. Blood LH concentration was determined by RIA and gonadotrope PR expression by immunohistochemistry. Results showed that i) EB and DPN potentiated the negative feedback of TX on basal LH release; ii) DPN reduced TX-induced PR expression; iii) EB and PPT blocked TX-elicited LHRH self-priming and iv) ZK299 reduced LHRH-stimulated LH secretion and blocked LHRH self-priming. These observations suggest that oestrogen action on LH secretion in the rat is exerted at the classic ERα pool and that this action might be modulated by both ERβ and membrane ERα through their effects on PR expression and action respectively.

Plasma β-endorphin and LH during prolonged hypoglycaemia in ewes

1993 ◽  
Vol 1993 ◽  
pp. 93-93 ◽  
Author(s):  
A.M.X. Eloy ◽  
R.G. Rodway
Keyword(s):  
Plasma Concentrations ◽  
Reproductive Function ◽  
Opioid Peptide ◽  
Inhibitory Effect ◽  
Elevated Plasma ◽  
Lh Release ◽  
Lh Secretion

Normal reproductive function in female animals can be drastically impaired by a variety of stressful stimuli. For example, undernutrition and hypoglycaemia in sheep have been shown to suppress pulsatile LH secretion and to reduce the number of ewes showing pre-ovulatory LH peaks (Crump and Rodway 1986, Clarke et al. 1990). Similar stresses are also known to cause release of the opioid peptide β-endorphin into the circulation. Opioids are well-known to have a central inhibitory effect on LH release, although whether the elevated plasma concentrations of these peptides have any effect on LH secretion is unclear. The present study investigated the affect of insulin-induced hypoglycaemia on plasma concentrations of β-endorphin and LH.

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

scholarly journals Gonadotrope oestrogen receptor-α and -β and progesterone receptor immunoreactivity after ovariectomy and exposure to oestradiol benzoate, tamoxifen or raloxifene in the rat: correlation with LH secretion

2005 ◽  
Vol 184 (1) ◽  
pp. 59-68 ◽  
Author(s):  
J E Sánchez-Criado ◽  
J Martín de las Mulas ◽  
C Bellido ◽  
R Aguilar ◽  
J C Garrido-Gracia
Keyword(s):  
Progesterone Receptor ◽  
Oestrogen Receptor ◽  
Immunohistochemical Expression ◽  
Stimulatory Action ◽  
Receptor Modulator ◽  
Ovx Rats ◽  
Oestradiol Benzoate ◽  
Cycle Dependent ◽  
Lh Secretion ◽  
Selective Oestrogen Receptor Modulator

The selective oestrogen receptor modulator (SERM) tamoxifen (TX) has agonist/antagonist actions on LH secretion in the rat. Whereas in the absence of oestrogens TX elicits progesterone receptor (PR)-dependent GnRH self-priming, it antagonizes oestrogen-stimulatory action on LH secretion. The aim of these experiments was to explore whether TX treatment-induced differential expression of oestrogen receptor (ER)α and ERβ in the gonadotrope may determine its agonist effect on LH secretion. In the first experiment, basal LH secretion, GnRH-stimulated LH secretion and PR-dependent GnRH self-priming were determined in incubated pituitaries from ovariectomized (OVX) rats treated with oestradiol benzoate (EB), TX or raloxifene (RX). Cycling rats in metoestrus or pro-oestrus were used as basic controls. As in pro-oestrus, pituitaries from OVX rats treated with EB exhibited GnRH-stimulated LH secretion, immunohistochemical PR expression and GnRH self-priming. While RX had no effect on these parameters, TX induced PR expression and GnRH self-priming. GnRH self-priming was absent in pituitaries incubated with the antiprogestin ZK299. In the second experiment, we evaluated the immunohistochemical expression of ERα and ERβ in gonadotropes of cycling rats and OVX rats treated with EB, TX or RX. We found that while ERα expression was similar in all six groups, ERα expression was oestrous cycle dependent. Moreover, ERα expression in gonadotropes of TX-treated rats was as high as that found in pro-oestrus, while ERα expression in the gonadotropes of RX-treated rats was lower than in metoestrous or pro-oestrous pituitaries. These results suggest that, in the absence of the cognate ligand, TX, unlike RX, may regulate LH secretion through the ERα subtype in gonadotropes.

Viral Antigen Distribution in Organs of Cattle Experimentally Infected with Rinderpest Virus

1993 ◽  
Vol 30 (6) ◽  
pp. 544-554 ◽  
Author(s):  
P. Wohlsein ◽  
G. Trautwein ◽  
T. C. Harder ◽  
B. Liess ◽  
T. Barrett
Keyword(s):  
Viral Antigen ◽  
Virulent Strain ◽  
Immunoperoxidase Method ◽  
Rinderpest Virus ◽  
Formalin Fixed Paraffin ◽  
Formalin Fixed Paraffin Embedded ◽  
The Central Nervous System ◽  
Distribution In Organs ◽  
Indirect Immunoperoxidase

The distribution of viral antigen in various organs of four approximately 10-month-old castrated male Friesian cattle experimentally infected with a highly virulent strain of rinderpest virus was studied. A monoclonal antibody with genus-specific reactivity for morbilliviruses was applied in an indirect immunoperoxidase method performed on formalin-fixed, paraffin-embedded tissue sections. Rinderpest viral antigen was located mainly in the cytoplasm of the epithelial cells of the digestive, respiratory, and urinary tracts, as well as in the cells of endocrine glands (adrenal, thyroid) and exocrine glands (salivary glands, sebaceous glands, exocrine pancreas). Furthermore, different types of cells in lymphatic organs contained rinderpest viral antigen. In contrast to the documented results of studies carried out with other morbilliviruses, tissues of the central nervous system did not contain viral antigen. Various types of epithelial and lymphoreticular cells are the main targets of a virulent strain of rinderpest virus in vivo.

Sign in / Sign up

Export Citation Format

Share Document