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PubMed1997

Progesterone-dependent decidualization of the human endometrium is mediated by cAMP.

Progesterone is a key factor in regulating endometrial cell decidualization, but the signal transduction pathways involved in mediating the effects of progesterone are not known. A role of the cAMP pathway in decidualization has been suggested by in vitro studies demonstrating that cAMP agonists can stimulate decidualization, in the absence of sex steroids. In this article, we have used an in vitro culture model of progesterone-dependent decidualization of human endometrial stromal cells to examine whether progesterone-induced decidualization is associated with activation of the cAMP signal transduction pathway in which the prolactin gene expression is a marker of decidualization. Following a lag period of approx 3 d, progesterone induced prolactin secretion and elevated intracellular cAMP levels. By d 15, cAMP and prolactin levels were approx 10- and 60-fold greater, respectively, than those on d 3. Changes in cAMP levels showed a positive correlation with prolactin secretion. Prostaglandin E2 (PGE2), which enhances progesterone-dependent decidualization, also increased both prolactin secretion and cAMP levels approx two- to fourfold on d 15 compared with d 3, whereas PGE2 alone, which does not induce decidualization, did not stimulate prolactin secretion or intracellular cAMP accumulation. Conversely, all-trans retinoic acid, which attenuates progesterone-dependent decidualization, significantly (p < 0.05) decreased both prolactin secretion and cAMP levels. Furthermore, the protein kinase A (PKA) inhibitor, 8-bromoadenosine-3',5'-cyclic monophosphorothioate, significantly (p < 0.05) suppressed progesterone-dependent prolactin expression. Since activation of the PGE2 receptor subtype EP2 stimulates adenylate cyclase, reverse transcription-polymerase chain reaction (RT-PCR) analysis of endometrial cells was undertaken. Expression of EP2 mRNA was induced in cells treated with progesterone and estradiol alone or with PGE2, compared with untreated controls. The data suggest that the cAMP signal transduction cascade is activated during progesterone-dependent decidualization.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2005

Progesterone pre-treatment potentiates EGF pathway signaling in the breast cancer cell line ZR-75.

Progesterone in hormone replacement therapy (HRT) preparations increases, while hysterectomy greatly reduces, the incidence of breast cancer. Cross-talk between the progesterone and growth factor signaling pathways occurs at multiple levels and this maybe a key factor in breast cancer survival and progression. To test this hypothesis, we characterized the effect of progesterone pre-treatment on the sensitization of the epidermal growth factor (EGF) signaling pathway to EGF in the breast cancer cell line ZR-75. For the first time in ZR-75 cells and in agreement with previous work using synthetic progestins, we demonstrate that pre-treatment with the natural ligand progesterone increases EGF receptor (EGFR) levels and subsequent ligand-dependent phosphorylation. Downstream we demonstrate that progesterone alone increases erk-1 + 2 phosphorylation, potentiates EGF-phosphorylated erk-1 + 2 and maintains these levels elevated for 24 h; over 20 h longer than in vehicle treated cells. Additionally, progesterone increased the levels of STAT5, another component of the EGF signaling cascade. Progesterone increased EGF mediated transcription of a c-fos promoter reporter and the nuclear localization of the native c-fos protein. Furthermore, progesterone and EGF both alone and in combination, significantly increase cell proliferation. Several results presented herein demonstrate the conformity between the action of the natural ligand progesterone with that of synthetic progestins such as MPA and R5020 and allows the postulation that the progestin/progesterone-dependent increase of EGF signaling provides a survival advantage to burgeoning cancer cells and may contribute to the breast cancer risk associated with endogenous progesterone and with progestin-containing HRT.

Breast Neoplasms↗
PubMed1986

A physiological dose of progesterone affects rat striatum biogenic amine metabolism.

Ovariectomized rats injected with progesterone (50 micrograms s.c.) showed a peak in striatum dopamine (DA) concentration after 15 min followed by a decrease at 60-75 min and a return to control values 90 min after the steroid injection. The DA metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were increased after the progesterone injection, with a peak at 45 min and a return to control values after about 2 h. Striatum serotonin (5-HT) concentrations remained unchanged after the progesterone injection while its metabolite 5-hydroxyindoleacetic acid (5-HIAA) was increased at 45 min and returned to control values after 2 h. The peak plasma progesterone concentration occurred 15-30 min after the steroid injection while estradiol concentrations were unchanged indicating no significant conversion of progesterone into estradiol. A similar experiment was performed in male rats. As with female rats, a progesterone injection led to a progesterone peak at 30 min while plasma estradiol levels remained unchanged. Male rats responded to the progesterone injection with a maximal increase of DA, DOPAC and HVA concentrations as soon as after 15 min and these amines remained elevated up to 75 min after the steroid injection. 5-HT and 5-HIAA remained unchanged after the progesterone injection. Thus, very small physiological doses of progesterone can increase striatum dopaminergic activity in rats of both sexes while serotonergic activity is influenced only in female rats. This effect is seen within minutes and is relatively short. It is probably non-genomic, presynaptic and similar to the effect of a small dose of a DA releasing agent.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Inhibition of the protective effect of estrogen by progesterone in experimental atherosclerosis.

The aim of the present study was to determine the effect of progesterone on the action of estrogen in the development of atherosclerosis. A total of 48 female New Zealand white (NZW) rabbits were ovariectomized. The animals were separated into 6 groups of 8 animals each and received subsequently a 0.5% cholesterol diet for 12 weeks. During this cholesterol feeding period, either estradiol (1 mg/kg body weight (BW)/week), progesterone (25 mg/kg BW/week), or combined estradiol/progesterone (in above dosages) was administered intramuscularly in each group (n = 8 each) of ovariectomized rabbits. One additional group of 8 animals received a combined estrogen/ progesterone regimen, but with progesterone at one third of the above mentioned dosage. In another 8 rabbits, progesterone was reduced to one ninth of the maximum dosage above, whereas estrogen was kept the same, at 1 mg/kg BW/week. Eight ovariectomized animals served as the control group and received no hormone treatment. After 12 weeks, the animals were sacrificed and the proximal aortic arch was removed for further histological examination. An inhibitory effect of estrogen of intimal thickening was found, in comparison to the control group (intimal area: 0.7 +/- 0.5 mm2 vs. 3.7 +/- 2.5 mm2, P < 0.01), whereas progesterone alone did not show a significant effect on intimal plaque size (intimal area: 4.0 +/- 2.3 mm2). In combination with progesterone (high dose), estrogen was not able to reduce intimal atherosclerosis (intimal area: 3.4 +/- 2.4 mm2). However, the beneficial effect of estrogen was not affected by progesterone, when this was reduced respectively to one third (intimal area: 0.8 +/- 0.7 mm2), or to one ninth of the highest dosage (intimal area: 0.6 +/- 0.4 mm2). Interestingly, these differences in atherosclerotic plaque development were observed without significant changes in plasma cholesterol concentrations by the administered hormones. In conclusion, progesterone was dose-dependently able to completely inhibit the beneficial effect of estrogen in experimental atherosclerosis, suggesting that progesterone exerts a direct inhibitory effect on the athero-protective action of estrogen. In the context of recently published data, the present work confirms the importance of the 'non-lipid-mediated', anti-atherosclerotic effect of estrogen, probably due to an interaction with six hormone receptors in vascular smooth muscle cells (VSMC).

Androgens↗
PubMed1984

A dual modulatory effect of progesterone on the LHRH-induced LH release.

The role of progesterone on the release of LH induced by 25 or 50 ng of LHRH was studied in proestrus rats in which spontaneous preovulatory release of LH was prevented by sodium pentobarbitone. After the s.c. administration of progesterone (5 mg) at 18.00 h of diestrus day 2 or at 12.00 h of proestrus, serum LH was not detectable at 17.15 h of proestrus. Injections of 25 or 50 ng of LHRH at 17.00 h of proestrus induced a dose response release of LH 15 min after. However, the LH response to LHRH administration increased significantly when progesterone was injected at 12.00 h of proestrus. The potentiating effect of progesterone seems to be exerted at pituitary level. The effect of LHRH and the enhanced response of the pituitary after progesterone treatment was prevented by the administration of the antiestrogen Tamoxifen in diestrus day 2. The release of LH induced by 50 ng of LHRH on proestrus day was blocked by the previous injection of progesterone on diestrus day 2. The inhibition was maintained even though a second dose of progesterone was given at 12.00 h of proestrus. The simultaneous administration of estrogen and progesterone on diestrus day 2 did not prevent the inhibitory effect of progesterone. It is concluded that the facilitatory or inhibitory effect of progesterone on the release of LH induced by LHRH is dependent upon the previous sensitization of the pituitary to estrogen.

Animals↗
PubMed1989

Effect of human chorionic gonadotropin and prostaglandin F2a on progesterone production by human luteal cells.

To determine and compare the direct effects of prostaglandin F2a (PGF2a) and human chorionic gonadotropin (hCG) on luteal cell progesterone production in vitro, 9 human corpora lutea obtained at tubal ligation were minced and treated with collagenase to disaggregate luteal cells. Dispersed luteal cells (80% viable) were incubated in air at 37 degrees C in a shaking water bath for 3 h and total progesterone in the media and cells was determined by radioimmunoassay. Optimum progesterone production was obtained using 25,000 or more cells per incubate and an incubation time of 2-4 h. hCG-stimulated progesterone production increased significantly with 0.01 IU to as high as 100 IU. In the early luteal phase (days 1-5 post ovulation or days 15-20 of the luteal phase), PGF2a (10-1000 ng) significantly inhibited progesterone production but significantly stimulated progesterone production in the mid-luteal phase (days 21-25). PGF2a had no effect on luteal cell progesterone production in the late luteal phase (days 26-30). This age-dependent direct effect of PGF2a on human luteal cell progesterone production in vitro indicates a role for PGF2a in the total intragonadal regulation of progesterone output, possibly through a paracrine or autocrine manner directed towards synchronizing luteal progesterone secretion and endometrial preparation for nidation.

Chorionic Gonadotropin↗
PubMed1989

Second messenger systems and progesterone secretion in the small cells of the bovine corpus luteum: effects of gonadotropins and prostaglandin F2a.

The present studies were conducted to determine the effects of gonadotropins (LH and hCG) and prostaglandin F2a (PGF2a) on the production of "second messengers" and progesterone synthesis in purified preparations of bovine small luteal cells. Corpora lutea were removed from heifers during the luteal phase of the normal estrous cycle. Small luteal cells were isolated by unit-gravity sedimentation and were 95-99% pure. LH provoked rapid and sustained increases in the levels of [3H]inositol mono-, bis-, and trisphosphates (IP, IP2, IP3, respectively), cAMP and progesterone in small luteal cells. LiCl (10 mM) enhanced inositol phosphate accumulation in response to LH but had no effect on LH-stimulated cAMP or progesterone accumulation. Time course studies revealed that LH-induced increases in IP3 and cAMP occurred simultaneously and preceded the increases in progesterone secretion. Similar dose-response relationships were observed for inositol phosphate and cAMP accumulation with maximal increases observed with 1-10 micrograms/ml of LH. Progesterone accumulation was maximal at 1-10 ng/ml of LH. LH (1 microgram/ml) and hCG (20 IU/ml) provoked similar increases in inositol phosphate, cAMP and progesterone accumulation in small luteal cells. 8-Bromo-cAMP (2.5 mM) and forskolin (1 microM) increased progesterone synthesis but did not increase inositol phosphate accumulation in 30 min incubations. PGF2a (1 microM) was more effective than LH (1 microgram/ml) at stimulating increases in inositol phosphate accumulation (4.4-fold vs 2.2-fold increase for PGF2a and LH, respectively). The combined effects of LH and PGF2a on accumulation of inositol phosphates were slightly greater than the effects of PGF2a alone. In 30 min incubations, PGF2a had no effect on cAMP accumulation and provoked small increases in progesterone secretion. Additionally, PGF2a treatment had no significant effect on LH-induced cAMP or progesterone accumulation in 30 min incubations of small luteal cells. These findings provide the first evidence that gonadotropins stimulate the cAMP and IP3-diacylglycerol transmembrane signalling systems in bovine small luteal cells. PGF2a stimulated phospholipase C activity in small cells but did not reduce LH-stimulated cAMP or progesterone accumulation. These results also demonstrate that induction of functional luteolysis in vitro requires more than the activation of the phospholipase C-IP3/calcium and -diacylglycerol/protein kinase C transmembrane signalling system.

Animals↗
PubMed1989

Progesterone can either increase or decrease weight gain and adiposity in ovariectomized Syrian hamsters.

We examined the effects of estradiol and progesterone on weight gain, food intake, and carcass composition in Syrian hamsters (Mesocricetus auratus). In ovariectomized (OVX) hamsters injections of 5 micrograms/day estradiol benzoate (EB) alone decreased weight gain and adiposity, whereas treatment with progesterone alone (1 or 5 mg/day) resulted in increased weight gain and adiposity. However, concurrent treatment with progesterone and EB reduced body fat content to levels significantly below those of hamsters treated with EB alone. In a second experiment, 17 beta-estradiol and progesterone were administered via subcutaneous Silastic capsules in doses which produce physiological levels of steroids. Implants of estradiol significantly decreased body weight gain and fat content. As in the first experiment, these effects of estradiol were exaggerated by concurrent progesterone administration. Implants of progesterone alone did not affect body weight or fatness in OVX hamsters. These data indicate that estradiol and progesterone interact to decrease body lipid stores in hamsters, whereas in rats progesterone reverses the adiposity-reducing actions of estradiol. This species difference in responses to progesterone could help to explain why rats increase, whereas hamsters decrease, their body lipid stores during pregnancy, when circulating progesterone levels are elevated.

Adipose Tissue↗
PubMed1979

The source of progesterone in preimplantation rabbit blastocysts.

In vitro and in vivo synthesis of progesterone, sequestration of progesterone from the surrounding medium, and its subsequent conversion to metabolites was investigated in 146 hr post coitus preimplantation rabbit blastocysts. No significant conversion of 3H-pregnenolone to 3H-progesterone was observed throughout the 8 hr incubation. Progesterone content in blastocysts and culture medium did not change during the course of an 8 hr incubation. This suggests that the failure to detect incorporation of label into progesterone was not due to the presence of a large endogenous pool of pregnenolone. Significant uptake (p less than 0.05) of 3H-progesterone from the incubation medium was observed as was significant conversion of the 3H-progesterone to unidentified metabolites. Therefore it would appear that the preimplantation rabbit blastocyst is not capable of de novo synthesis of progesterone from pregnenolone prior to implantation but sequesters progesterone from the surrounding medium and converts it to progesterone metabolites.

Animals↗
PubMed1988

Effect of exogenous progesterone on prostaglandin F2 alpha release and the interestrous interval in the bovine.

The present study was developed to determine if administration of progesterone, early in the estrous cycle of the cow, stimulated an advanced pulsatile release of PGF2 alpha from the uterine endometrium resulting in a decreased interestrous interval. Twenty-three cyclic beef cows were randomly assigned to receive either sesame oil or progesterone (100 mg) on Day 1, 2, 3 and 4 of the estrous cycle. Peripheral plasma concentrations of progesterone and the metabolite of prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha (PGFM) were measured by radioimmunoassay. Administration of exogenous progesterone increased peripheral plasma concentration of progesterone in treated (3.67 ng/ml) compared to control (1.28 ng/ml) cows from Day 2 through 5 of the estrous cycle. Progesterone administration shortened the interestrous interval (16.7 d) compared to controls (21.6 d). The shortened interestrous intervals in treated cows resulted from an earlier decline in peripheral plasma progesterone. Decline of peripheral plasma progesterone concentrations is coincident with an increased pulsatile release of PGFM in both progesterone treated and control cows. Results indicate that administration of exogenous progesterone stimulates an earlier maturation of endometrial development, causing an advanced release of PGF2 alpha which shortens the interestrous interval of the cow.

Animals↗
PubMed1988

A comparison of the effects of cyclooxygenase prostanoids on progesterone production by small and large bovine luteal cells.

Highly purified preparations of small and large bovine luteal cells were utilized to examine the effects of prostaglandins F2 alpha (PGF2 alpha), E2 (PGE2) and I2 (PGI2) analog on progesterone production. Corpora lutea were obtained from Holstein heifers between days 10 and 12 of the estrous cycle. Purified small and large cells were obtained by unit gravity sedimentation and flow cytometry. Progesterone accumulation was determined in 1 x 10(5) small and 5 x 10(3) large cells after 2 and 4 h incubations respectively. Progesterone synthesis was increased (p less than 0.05) in the small cells by the increasing levels of PGF2 alpha, PGE2, carba-PGI2 and LH. PGF2 alpha, but not PGE2 or carba-PGI2 increased (p less than 0.05) LH-stimulated progesterone production. There was no interaction of various combinations of prostaglandins on progesterone production in the small cells. In the large cells, PGF2 alpha had no effect on basal progesterone production. However, it inhibited LH-stimulated progesterone synthesis. In contrast, PGE2 and carba-PGI2 stimulated (p less than 0.05) basal progesterone production in the large cells. In the presence of LH, high levels of carba-PGI2 inhibited (p less than 0.05) progesterone synthesis. The PGE2 and PGI2-stimulated progesterone production in the large luteal cells was also inhibited in the presence of PGF2 alpha. These data suggest all of the prostaglandins used exert a luteotropic action in the small cells. In the large cells only PGE2 and carba-PGI2 are luteotropic, while PGF2 alpha exerts a luteolytic action. The effects of the prostaglandins in the small and large luteal cells suggest that their receptors are present in both cell types.

Animals↗
PubMed1975

An analysis of the binding of the chick oviduct progesterone-receptor to chromatin.

The binding of progesterone-receptor complexes to chromatin from target and nontarget tissues was studied in vitro. Chromatin from both target and nontarget tissues responds in a similar manner to saly and cofactors and has the same K(D) (approx. 3.10(-9) M) for the progesterone-receptor complex. The only observed difference in the binding of the progesterone-receptor complex to target and nontarget chromatins is the difference in total number of acceptor sites. oviduct chromatin has approx. 1300 sites/pg DNA, spleen chromatin has approx. 840 sites/pg DNA, and erythrocyte chromatin has about 330 sites/pg DNA. The K(D) and number of acceptor sites for progesterone-receptor complex binding to oviduct chromatin remains the same even after extensive purification of the progesterone-receptor complex. Activation of cytosol labeled with [3H]progesterone by preincubation at 25 degrees C, analogous to that required for maximal nuclear binding, occurs if the binding studies to chromatin are performed in 0.025 M salt. The absence of an observable temperature effect when the studies are performed at 0.15 M salt is due to the activation of the receptor by salt. The dissociation of the progesterone-receptor complex from chromatin exhibits a single dissociation rate and the initial event is the appearance of free progesterone rather than a progesterone-receptor complex. Lastly, the treatment of chromatin with an antibody prepared against either single-stranded DNA or double-stranded DNA does not alter the extent of binding of the progesterone-receptor complex. Similarly, pretreatment of chromatin with a single-stranded nuclease does not inhibit the capacity of chromatin to bind the hormone-receptor complex.

Animals↗
PubMed1992

Presence of calbindin and lack of parvalbumin in progesterone receptor-containing neurons of the monkey mediobasal hypothalamus.

All of the progesterone receptor-containing cells of the monkey hypothalamus are GABAergic. The aim of this study was to further characterize these GABAergic progesterone receptor-containing neurons based on their calbindin or parvalbumin content. These calcium-binding proteins are characteristic markers of different populations of GABAergic neurons in the central nervous system. Double-immunolabeling for progesterone receptor and either calbindin or parvalbumin was performed on hypothalamic Vibratome sections of estrogen primed African green monkeys (Cercopithecus aethiops). Progesterone receptor-containing calbindin-immunoreactive neurons were observed in the ventromedial and periventricular areas of the hypothalamus. Forty-one per cent of the progesterone receptor-containing cells in this area were calbindin immunopositive. No double-immunolabeled neurons could be detected in the infundibular (arcuate) nucleus. In tissue double-immunolabeled for progesterone receptor and parvalbumin, none of the progesterone receptor-containing neurons exhibited immunoreactivity for parvalbumin. Electron microscopic double-immunostaining for progesterone receptor and calbindin confirmed the light microscopic results. Furthermore, a large number of asymmetric synaptic contacts were observed on the calbindin-immunoreactive neurons. These observations demonstrate that progesterone receptor-containing cells in the monkey mediobasal hypothalamus consist of at least two different types of GABA neurons, and indicate that progesterone receptor-containing calbindin cells may be postsynaptic targets of excitatory fibers.

Animals↗
PubMed1996

Reproductive phenotpes of the progesterone receptor null mutant mouse.

Although progesterone has been traditionally associated with the establishment and maintenance of mammalian pregnancy, a number of studies have implicated physiological roles of this steroid hormone in other reproductive events. At present most of the downstream molecular and cellular mechanisms by which progesterone exerts its effects are unclear; however, the progesterone signal is known to be mediated initially by the progesterone receptor (PR), a member of the nuclear receptor superfamily of transcription factors. In most tissues studied, the PR is induced by ovarian estrogen via the estrogen receptor (ER), thereby implying that many of the observed reproductive physiological responses attributed to PR could conceivably be due to the combined effects of progesterone and estrogen. Therefore, to define clearly the distinct roles of progesterone and estrogen in vivo and to understand better progesterone function in a physiological context, we recently have generated a novel mouse strain in which both forms of the PR were ablated using gene targeting/embryonic stem cell techniques. Surprisingly, both male and female embryos, homozygous for the PR null mutation, developed to adulthood at the normal Mendelian frequency with no deviation in the sex ratio. Although developmental defects have yet to be detected in the adult male PR homozygote, extensive reproductive abnormalities were observed in the female. The reproductive phenotypes consisted of an inability to ovulate, uterine hyperplasia and inflammation, severely limited mammary gland development and an impairment in the induction of a sexual behavioral response. Collectively, these results provide direct in vivo evidence for progesterone's role as a pleiotropic coordinator of diverse reproductive events that together ensure female fertility. Finally, we believe that this animal model will be an invaluable tool in exploring the effects of progesterone in physiological systems other than reproduction and may, in the future, help to redefine progesterone not just as a sex steroid hormone but also as a key regulator of diverse physiological processes.

Animals↗
PubMed2004

Regulation of frequency of luteinizing hormone pulses by magnitude of acute change in circulating concentration of progesterone of female cattle.

The hypothesis was the greater the magnitude of acute increase in circulating concentration of progesterone of female cattle, the greater the acute inhibitory effect on frequency of pulsatile LH release. From Day 0 to 4 of the treatment period, females without functional corpora lutea were treated with varying doses of progesterone to result in varying concentrations of progesterone within the typical physiological range in blood. From Day 4 to 7, cattle were treated with a single dose of progesterone to achieve a similar circulating concentration of progesterone among all females in the study. Therefore, from Day 0 to 4 relative to Day 4 to 7 of the treatment period, females had a: (1) large (3.1 ng/ml), (2) moderate (2.5 ng/ml), or (3) small (0.5 ng/ml) increase in concentration of progesterone in blood. Frequency of LH pulses was greater (P <0.10) in females with the greatest magnitude of change in concentration of progesterone during the first 24 h following the change in concentration as compared with females with the moderate or small of change in concentration of progesterone suggesting our working hypothesis should be rejected. The greater the magnitude of acute change in concentration of progesterone, however, the longer time required for re-initiation of release of LH pulses of the amplitude of pulses that preceded the change in concentration of progesterone.

Animals↗
PubMed2006

Estradiol and progesterone modulation of angiotensin II receptors in the arcuate nucleus of ovariectomized and lactating rats.

The expression of angiotensin II (Ang II) receptors in the brain is modulated by estradiol and progesterone. Considering that Ang II plays a critical role in controlling prolactin secretion and that neurons in the arcuate nucleus (ARC) are the main regulator of this function, the present study aimed to evaluate ARC Ang II receptor binding in 2 experimental models with different estradiol and progesterone plasma levels. Animals were divided into 4 groups: ovariectomy (OVX) plus oil vehicle, OVX plus estradiol and progesterone replacement, lactating rats on day 7 postpartum, and lactating rats on day 20. Animals were killed by decapitation, and the brains were removed. Ang II receptors were quantified by autoradiography in ARC. Trunk blood samples were collected, and plasma estradiol and progesterone were measured by radioimmunoassay. Treatment of OVX rats with estradiol and progesterone increased Ang II receptor binding when compared to OVX vehicle-treated animals. Plasma estradiol (r = +0.77) and progesterone (r = +0.87) were highly correlated with Ang II receptors in ovariectomized animals. Lactating rats (day 20) showed a significant decrease in Ang II receptor binding and plasma progesterone when compared to lactating rats (day 7), however, no difference was seen in plasma estradiol. Plasma levels of progesterone (r = +0.81), but not estradiol (r = +0.32), were highly correlated with Ang II receptors in lactating rats. In conclusion, present results show that ARC Ang II receptors decreases on day 20 of lactation compared to day 7 and are highly correlated with plasma progesterone, indicating a pivotal role for progesterone in this regulation.

Animals↗
PubMed2004

Progesterone inhibition of dopamine-induced increase in frequency of spontaneous excitatory postsynaptic currents in rat prelimbic cortical neurons.

We examined the effects of progesterone on frequency of miniature excitatory postsynaptic currents (mEPSCs) and spontaneous excitatory postsynaptic currents (sEPSCs), and dopamine-induced increase in the frequency of sEPSCs in pyramidal cells of layers V-VI of the rat prelimbic cortex using whole-cell patch-clamp techniques in slices. The results showed that progesterone 100 microM had no effects on the frequency of mEPSCs and sEPSCs, but significantly inhibited dopamine-induced increase in frequency of sEPSCs. This was in contrast to the effect of progesterone on the effect of 5-HT, which showed no changes after progesterone. When studying the mechanism of the progesterone effect, we observed that GABA(A) receptor antagonist and progesterone receptor antagonist did not influence the effect of progesterone; progesterone had no effects on D1 receptor agonist, protein kinase A and protein kinase C activator-induced increase in the frequency of sEPSCs. Interestingly, sigma(1) receptor antagonist could inhibit the effect of dopamine and sigma(1) receptor agonist had a synergistic effect on the effect of D1 receptor agonist. These results suggest that progesterone may inhibit dopamine-induced increase in frequency of sEPSCs in rat prelimbic cortical neurons via inhibition of sigma(1)/D1 receptor synergism because progesterone has been known to be an antagonist of sigma(1) receptor.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2006

Cerebellum progesterone concentration decreased in canine distemper virus infection.

Progesterone has neuroprotective effects including augmentation of myelination in the central and peripheral nervous system. This study was designed to determine if demyelinating lesions in the cerebellum resulting from canine distemper virus (CDV) infection are associated with progesterone levels. Progesterone was measured using radioimmunoassay in samples of the cerebellum, corpus callosum, medulla oblongata, parietal, frontal, temporal, and occipital cortices as well as cerebrospinal fluid (CSF) and plasma collected from ten CDV infected and six non-infected dogs. The cerebellum progesterone level was significantly different between CDV infected (0.66+/-0.09 ng/g) and control dogs (1.14+/-0.09 ng/g) (p<0.001); however, no difference was observed for the other CNS regions, plasma and CSF (p>0.05). The cerebellum progesterone level was also significantly different between acute (0.71+/-0.0 5 ng/g) and chronic cases (0.61+/-0.09 ng/g) (p<0.05). The CDV infected cerebella were also categorized histopathologically according to the severity of demyelinating lesions as mild (n=5), moderate (n=2), or severe (n=3) among which the cerebellum progesterone level was significantly different (p<0.05). Progesterone concentration was 0.71+/-0.05 ng/g in mild, 0.65+/-0.10 ng/g in moderate, and 0.56+/-0.07 ng/g in severe cases. In conclusion, progesterone concentration decreases in the cerebellum in CDV infection and the severity of demyelinating lesions is the greatest in cerebella with the lowest progesterone concentrations. The results suggest that local impairment of progesterone metabolism may be associated with the initiation and progression of cerebellar lesions in CDV infection.

Animals↗