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J D Blaustein

Publications and source records attributed to J D Blaustein.

At least 91 records · Page 5Linked to original sources
PubMed1987

The alpha 1-noradrenergic antagonist prazosin decreases the concentration of estrogen receptors in female rat hypothalamus.

A series of experiments was performed to determine the effects of the alpha 1-noradrenergic antagonist, prazosin, on the concentration of estrogen receptors in female rat brain and pituitary gland. Prazosin caused a dose-dependent decrease in the concentration of cytosol estrogen receptors in mediobasal hypothalamus when injected 10 and 16 h prior to assay. The drug was without effect on the concentration of nuclear estrogen receptors in the absence of estradiol, indicating that the decreased concentration of cytosol estrogen receptors is not due to nuclear estrogen receptor accumulation. Scatchard analysis confirmed that prazosin treatment decreases the concentration of cytosol estrogen receptors without influencing the apparent affinity of the receptors for [3H]estradiol. The prazosin-induced decrease in the concentration of cytosol estrogen receptors in the mediobasal hypothalamus was transient with maximal effects occurring between 8 and 12 h after a single injection. Competition analysis confirmed that prazosin is not an effective competitor for binding to the estrogen receptor in vitro. The effects of prazosin on the estrogen receptor system could not be attributed to modulation of the levels of norepinephrine or dopamine. Assay of the levels of norepinephrine and dopamine in hypothalamus and preoptic area after prazosin injection revealed no effects of prazosin on the level of either of these catecholamines. An estradiol injection resulted in the predicted decrease in the concentration of estrogen receptors accumulating in hypothalamic cell nuclei, suggesting that the cytosol estrogen receptors that decrease in concentration are functional receptors. Prazosin treatment did not result in a decrease in the effectiveness of estradiol in the induction of cytosol progestin receptors in the mediobasal hypothalamus, suggesting that the cells are regulated by the alpha 1-noradrenergic system may not be those cells in which progestin receptors are also induced. These experiments provide further evidence that the noradrenergic system modulates the concentration of estrogen receptors, and perhaps sensitivity to estradiol, in some cells within the rat hypothalamus.

Adrenergic alpha-Antagonists↗
PubMed1987

Noradrenergic regulation of cytosol estrogen receptors in female rat hypothalamus: possible role of alpha 2-noradrenergic receptors.

Because of the previous work demonstrating that the alpha 1-noradrenergic receptor antagonist, prazosin, decreases the concentration of cytosol estrogen receptors in rat mediobasal hypothalamus, a series of experiments was performed to determine the specificity of this effect to the alpha 1-noradrenergic system. Injection of the alpha 2-noradrenergic antagonist, yohimbine, caused a decrease in the concentration of estrogen receptors in mediobasal hypothalamus. In addition, the down-regulation of cytosol estrogen receptors by either the alpha 1-noradrenergic antagonist, prazosin, or the alpha 2-noradrenergic antagonist, yohimbine, could be blocked by pretreatment with the alpha 2-noradrenergic agonist, clonidine. The alpha 1-noradrenergic agonist, phenylephrine, was ineffective in blocking the effects of the alpha 1-noradrenergic antagonist, prazosin. These results add further support to the hypothesis that the alpha-noradrenergic system modulates the concentration of cytosol estrogen receptors in the rat hypothalamus. They suggest that the modulation may occur by way of alpha 2-noradrenergic receptors in addition to, or instead of, alpha 1-noradrenergic receptors.

Animals↗
PubMed1987

Small apomorphine-induced increase in the concentration of cytosol estrogen receptors in female rat hypothalamus and pituitary.

A series of experiments was performed to investigate the previously-reported modulation of estradiol binding in female rat brain and pituitary gland by drugs that influence the dopaminergic system. Injection of the dopamine agonist, apomorphine, at minimum doses of 1-2 mg/kg body weight caused slight increases (in most cases, less than 10%) in the concentration of cytosol estrogen receptors in the mediobasal hypothalamus and anterior pituitary gland without influencing the concentration in the preoptic area. However, after subsequent injection of a saturating dose of estradiol, the level of nuclear estrogen receptors accumulating did not differ significantly between apomorphine-treated animals and vehicle-injected controls. These results extend, in part, previous reports that have shown an apomorphine-induced increase in the concentration of [3H]estradiol in brain and pituitary cell nuclei after an injection of [3H]estradiol. However, we failed to observe differences in the concentration of cytosol estrogen receptors as large as would be expected by previous work, and we failed to observe differences in the concentration of nuclear estrogen receptors after estradiol injection.

Animals↗
PubMed1987

Estrogen-induced and estrogen-facilitated female rat sexual behavior is not mediated by progestin receptors.

Although sexual behavior during the rat estrous cycle is dependent on estradiol and progesterone, under some conditions, it can be induced by treatment with estradiol alone. Either chronic exposure to estradiol (estrogen-induced sexual behavior) or an acute large injection of estradiol in estradiol-primed rats (estrogen-facilitated sexual behavior) is capable of inducing sexual receptivity. It has been suggested that this progesterone-independent sexual behavior is referable to estradiol interaction with neural progestin receptors. A series of experiments was performed to investigate the possible dependence of estrogen-induced and estrogen-facilitated sexual behavior on neural progestin receptors. In the first series of experiments, the progesterone antagonist, RU 486, which inhibits progesterone-facilitated sexual behavior by interaction with progestin receptors, was injected into rats that were sexually receptive as a result of continuous exposure to estradiol. In the second series of experiments, RU 486 was injected prior to or following an acute large dose of estradiol (1 mg) in an attempt to block estradiol-facilitated lordosis. Although RU 486 was effective in inhibiting progesterone-facilitated sexual behavior in an identical procedure, in no case was RU 486 effective in inhibiting sexual behavior induced by estradiol alone. These findings, together with the fact that rats in which sexual behavior is facilitated by estradiol show much lower levels of soliciting behaviors than progesterone-facilitated rats, suggest that estradiol does not facilitate sexual behavior through the same mechanism as progesterone.

Animals↗
PubMed1987

Maintenance of progesterone-facilitated sexual behavior in female rats requires continued hypothalamic protein synthesis and nuclear progestin receptor occupation.

The role of ongoing progesterone-directed protein synthesis and hypothalamic cell nuclear progestin receptor occupation in maintaining the duration of the period of sexual receptivity was determined in ovariectomized rats treated with 500 micrograms progesterone 44 h after receiving 2 micrograms estradiol benzoate. Injection of the protein synthesis inhibitor anisomycin (100 mg/kg BW) either 2 or 10 h after progesterone treatment resulted in decreased levels of both receptive and proceptive sexual behavior. Similarly, injection of RU 486, an antiprogestin, 2, 6, or 10 h after progesterone injection resulted in inhibition of sexual behavior within 4-8 h after administration. Using a modified cell nuclear isolation technique for the exchange assay of nuclear-bound progestin receptors, elevated levels of progestin binding in hypothalamic cell nuclear fractions were detected as late as 14 h after progesterone injection. By 18 h after progesterone injection, nuclear progestin receptor levels had returned to baseline, a time when the period of sexual behavior had terminated in similarly treated animals. These data suggest that continued progesterone action in hypothalamic cell nuclei is required for the maintenance of progesterone-facilitated sexual behavior in the female rat. Furthermore, they suggest that progesterone action maintains sexual responsiveness by altering the synthesis of a short-lived protein or set of proteins.

Animals↗
PubMed1986

Abbreviation of the period of sexual behavior in female guinea pigs by the progesterone antagonist RU 486.

In previous studies we have tested the hypothesis that the termination of the period of sexual behavior in female guinea pigs results from the loss of progestin receptors from hypothalamic cell nuclei. We have shown that hormonal manipulations that delay heat termination also delay loss of hypothalamic nuclear progestin receptors. In order to determine if accelerated nuclear receptor loss results in abbreviation of the period of sexual behavior, we tested the effect of 17 beta-hydroxy-11 beta-(4-dimethylaminophenyl)-17 alpha-(1-propyl)-estra-4,9-diene-3-one (RU 486), a progesterone antagonist, on heat termination. Ovariectomized guinea pigs were treated with estradiol benzoate. Forty hours later, they received progesterone followed 4 h later by injection of RU 486 or vehicle. RU 486 injected 4 h after progesterone caused heat abbreviation. We have found that RU 486 administration to estradiol-treated guinea pigs causes accumulation of progestin receptors in cell nuclear extract. Because this accumulation can be detected only when assay conditions are used that promote exchange of RU 486 progestin receptor complexes (15 degrees C incubation rather than 0 degree C); our routine assay conditions (at 0 degree C) can be used to measure primarily receptors that are occupied by progesterone. In order to confirm that RU 486 decreased progesterone-occupied nuclear progestin receptor levels when injected 4 h after progesterone, animals treated as in the behavioral experiment were killed 6 or 10 h after progesterone injection (2 or 6 h after RU 486), and nuclear progestin receptor levels were measured. RU 486 treatment resulted in lowered nuclear concentrations of hypothalamic progestin receptors at both times. These results support our hypothesis that the termination of the period of sexual receptivity in female guinea pigs is the result of loss of progestin receptors from hypothalamic cell nuclei.

Animals↗
PubMed1986

Hypothalamic nuclear progestin receptors and the duration of sexual receptivity in ovariectomized and ovariectomized-hysterectomized rats.

In order to determine if the enhancement of sexual behavior in hysterectomized rats is associated with an increased level of hypothalamic nuclear progestin receptors, ovariectomized (OVX) and ovariectomized-hysterectomized (OVHX) rats were injected with 2 micrograms estradiol benzoate. Twenty-four hr later, animals were injected with 0.5 mg progesterone and were tested for sexual receptivity every 4 hr. Hysterectomy had an overall facilitatory effect on lordosis and increased the duration of the period of sexual receptivity by about 4 hr. In a second experiment, similarly-treated animals were killed 4, 8, or 12 hr after progesterone injection, and hypothalamic nuclear progestin receptor levels were measured. In contrast to what has been reported for guinea pigs, nuclear progestin receptor levels decreased to baseline 8-12 hr before the termination of sexual receptivity. Nuclear progestin receptor concentrations were higher in OVHX rats than in OVX rats at 4 hr after progesterone injection, and there was a trend toward higher receptor concentrations in OVHX rats at 8 hr. These results demonstrate that hysterectomy-induced facilitation of sexual receptivity is associated with an increased level of hypothalamic nuclear progestin receptors. Furthermore, they suggest a fundamental difference in the regulation of nuclear progestin receptor retention between rats and guinea pigs.

Animals↗
PubMed1986

Cell nuclear accumulation of estrogen receptors in rat brain and pituitary gland after treatment with a dopamine-beta-hydroxylase inhibitor.

In a recent experiment, it was found that the dopamine-beta-hydroxylase inhibitor, U-14,624, decreases the concentration of cytosol progestin receptors in guinea pig hypothalamus and causes an increase in the concentration of nuclear progestin receptors. In this series of experiments, the possibility that similar effects would be seen in the rat estrogen receptor system in mediobasal hypothalamus and pituitary was tested. U-14,624 caused a time-dependent decrease in the concentration of cytosol estrogen receptors and increase in the concentration of nuclear estrogen receptors in both mediobasal hypothalamus and anterior pituitary gland in ovariectomized rats, both in the absence and presence of low levels of estradiol, as well as in ovariectomized-adrenalectomized rats. The nuclear estrogen receptors that accumulate after U-14,624 injection do not require incubation at 25 degrees C to be assayed, suggesting that they are not occupied by an estradiol-like ligand. The nuclear estrogen receptors that accumulate after U-14,624 treatment are high affinity, with an apparent dissociation constant of approximately 0.1 nM. U-14,624 does not compete with (3H)estradiol, in vitro, suggesting that it does not directly interact with estrogen receptors. These results suggest that under some conditions, inhibition of dopamine-beta-hydroxylase causes a modification in unoccupied estrogen receptors so that they develop a higher affinity for cell nuclear components.

Adrenalectomy↗
PubMed1986

Some catecholamine inhibitors do not cause accumulation of nuclear estrogen receptors in rat hypothalamus and anterior pituitary gland.

We have recently shown that the dopamine-beta-hydroxylase inhibitor, U-14,624, decreases the concentration of cytosol estrogen receptors in the mediobasal hypothalamus (MBH) and anterior pituitary gland (AP) in ovariectomized rats, but that it also causes cell nuclear accumulation of estrogen receptors. We tried to determine if this is the mechanism by which other catecholaminergic inhibitors decrease the concentration of cytosol estrogen receptors in either the MBH or AP. The previously reported decrease in the concentration of cytosol estrogen receptors in AP by the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine was confirmed. Also, the decrease in the concentration of cytosol estrogen receptors in MBH after treatment with the dopamine-beta-hydroxylase inhibitors, diethyldithiocarbamate and FLA 63 was demonstrated. In no case was an increase in the concentration of nuclear estrogen receptor accumulation detected after treatment with the drugs. Results of assays of norepinephrine and dopamine levels in MBH after the various treatments suggest that, at the dosage used, U-14,624 has a greater effect on norepinephrine and dopamine levels that the other dopamine-beta-hydroxylase inhibitors. The results of these experiments suggest that inhibitors of dopamine-beta-hydroxylase and tyrosine hydroxylase cause decreases in the concentration of cytosol estrogen receptors in either the MBH or AP that are not referable to increased cell nuclear accumulation of estrogen receptors.

Animals↗
PubMed1986

Dopamine-beta-hydroxylase inhibitors modulate the concentration of functional estrogen receptors in female rat hypothalamus and pituitary gland.

In order to study further the regulation of steroid hormone receptors in the brain and anterior pituitary gland of ovariectomized rats by catecholamines, the influence of two dopamine-beta-hydroxylase inhibitors on the estrogen receptor system was studied. The two inhibitors, FLA 63 and diethyldithiocarbamate (DDC) both caused a biphasic effect on the concentration of cytosol estrogen receptors in the mediobasal hypothalamus without influencing the concentration of cell nuclear estrogen receptors in the absence of estradiol; the concentration of cytosol estrogen receptors first increased and then decreased after treatment. In a study of the neuroanatomical areas in which inhibition of dopamine-beta-hydroxylase decreases the concentration of cytosol estrogen receptors, it was found that the concentration of cytosol estrogen receptors decreased after drug treatment in the mediobasal hypothalamus and preoptic area-septum, but not in the amygdala. This suggests that the decrease in concentration of hypothalamic cytosol estrogen receptors caused by dopamine-beta-hydroxylase inhibitors is not a nonspecific effect on all cytosol estrogen receptors. Finally, an injection of estradiol-17 beta in animals that had been pretreated with either DDC or FLA 63 resulted in less accumulation of cell nuclear estrogen receptors in those tissues in which the drug first caused a decrease in the concentration of cytosol estrogen receptors than in vehicle-injected controls. Therefore, under some conditions, pretreatment with a dopamine-beta-hydroxylase inhibitor decreased the concentration of functional cytosol estrogen receptors resulting in decreased nuclear estrogen receptor accumulation in response to an estradiol injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Loss of hypothalamic nuclear-bound progestin receptors: factors involved and the relationship to heat termination in female guinea pigs.

The hypothesis that the termination of sexual receptivity (heat) in female guinea pigs results from loss of progestin receptors from hypothalamic cell nuclei was tested. First, we attempted to find an optimal dose of progesterone that would result in a prolonged period of sexual receptivity. Ovariectomized guinea pigs were implanted with 10% estradiol capsules. Forty hours later, each received one of several sized progesterone capsules before being tested hourly for lordosis. Surprisingly, none of the progesterone doses resulted in delayed heat termination. In order to determine whether elevated levels of estradiol and progesterone maintain elevated levels of nuclear progestin receptors despite the lack of effect on heat duration, animals were treated as described above except that only one size progesterone capsule (3.0 cm) or an empty capsule was implanted. Despite elevated serum progesterone concentrations, nuclear progestin receptor levels decreased gradually and approached control levels at about the same time as heat termination had occurred in similarly-treated animals. Cytosol progestin receptor levels decreased following progesterone treatment and remained lowered at all times measured. In order to further investigate the relationship between blood progesterone concentrations and retention of nuclear progestin receptors we decreased blood progesterone concentrations by removing progesterone capsules 2 h following insertion. Nuclear progestin receptor levels declined gradually concurrent with a decline in serum progesterone levels in animals exposed to progesterone capsules for only 2 h. In animals exposed to capsules continuously, nuclear progestin receptor levels again decreased but at a slightly slower rate. In order to test the effect of progesterone capsule removal on female sexual behavior, ovariectomized guinea pigs were treated as described and tested hourly for lordosis. Fewer animals in the group exposed to progesterone capsules for 2 h became sexually receptive as compared to animals continuously-exposed to progesterone capsules. Of those animals that did respond, heat termination had occurred by the same time that nuclear progestin receptor levels had returned to control levels in similarly-treated animals. These experiments support the hypothesis that heat termination results from the loss of progestin receptors from hypothalamic cell nuclei. In addition, they demonstrate that circulating progesterone levels play a role in regulating nuclear progestin receptor retention.

Animals↗
PubMed1985

Noradrenergic inhibitors cause accumulation of nuclear progestin receptors in guinea pig hypothalamus.

A series of experiments was performed to study the possible behavioral relevance of the apparent regulation of hypothalamic cytosol progestin receptors by noradrenergic transmission in female guinea pigs. In the first experiment, ovariectomized guinea pigs were injected with estradiol benzoate followed 36 h later by the dopamine-beta-hydroxylase inhibitor, U-14,624 or vehicle. Twelve h later, they were injected with progesterone and tested hourly for sexual behavior. Six h after the progesterone injection, a time at which inhibition of sexual behavior by the U-14,624 was confirmed, they were killed, and cytosol and nuclear progestin receptors were assayed in the hypothalamus and cerebral cortex. No difference was seen in the concentration of progestin receptors after drug treatment in these animals that also received a progesterone injection. In subsequent experiments, it was found that the U-14,624-inhibition of progesterone-facilitated sexual behavior is not accompanied by an inhibition of nuclear progestin receptor accumulation. Furthermore, it was found that the decreased cytosol progestin receptor level caused by U-14,624 prior to progesterone injection was accompanied by an increase in the concentration of nuclear progestin receptors. The increase in nuclear progestin receptors was also seen after treatment with the alpha-adrenergic antagonist, prazosin, U-14,624 does not compete with [3H]R 5020 for binding to the progestin receptor, suggesting that it does not directly cause translocation of progestin receptors. The results of these experiments suggest that the decrease in the concentration of cytosol progestin receptors caused by noradrenergic inhibitors is not due entirely to an interference with the formation of cytosol progestin receptors. Rather, it seems that these drugs, in some way, also cause the accumulation of progestin receptors in cell nuclei. Furthermore, they suggest that the mechanism by which these drugs inhibit sexual behavior may not be by interference with the progestin receptor system.

Animals↗
PubMed1984

Progesterone decreases the concentration of hypothalamic and anterior pituitary estrogen receptors in ovariectomized rats.

In a study of cellular mechanisms of progesterone's antiestrogenic action on behavior and neuroendocrine responses, we investigated the influence of progesterone on the concentration of estrogen receptors in the hypothalamus-preoptic area (HP), anterior pituitary gland (AP), and uterus of chronically estradiol-treated ovariectomized rats. Ovariectomized (OVX) rats were implanted s.c. with 15 mm silastic capsules of estradiol. One week later, they were injected with progesterone or oil vehicle and killed 6 h or 24 h later. Confirming previous reports, progesterone caused a decrease in the concentration of uterine cytosol and nuclear estrogen receptors at both times. Less consistent results were obtained in HP and AP; a decrease in the concentration of HP cytosol estrogen receptors was detected at 6 h, as was a small decrease in the concentration of HP nuclear estrogen receptors at 24 h. More consistent results were seen when a low priming dose of estradiol was used. Although progesterone was without effect on the concentration of nuclear estrogen receptors in HP and AP at 6 h, cytosol receptor levels were depressed by 25% in HP and 14% in AP. At 24 h after progesterone injection, nuclear estrogen receptor levels were decreased in all tissues, while cytosol estrogen receptor levels remained depressed. A study of the time course of progesterone's suppression of cytosol estrogen receptor concentration revealed that the effect is transient, occurring by 6 h after progesterone injection, but returning to baseline by 48 h after injection. Scatchard analysis confirmed that the decreased concentration of cytosol binding in HP was due to a decrease in the concentration of binding sites. As with nearly all of progesterone's neuroendocrine effects, the suppression of estrogen receptor levels requires estrogen priming. HP and AP cytosol from progesterone-treated rats did not seem to contain an estrogen receptor-regulatory factor as do uterine cell nuclei; loss of binding sites at 37 degrees C was no faster in cytosol from progesterone-treated rats. These results demonstrate that, under some conditions, progesterone decreases HP and AP estrogen receptor concentrations. Unlike progesterone's action in the uterus, the primary effect in the brain and pituitary gland seems to be on the cytosol receptor.

Animals↗
PubMed1984

Inhibition of sexual behavior in female guinea pigs by a progestin receptor antagonist.

The new steroidal progestin receptor antagonist, RU 38486, was used to determine if progesterone-facilitation of sexual behavior in female guinea pigs requires interaction of the hormone with neural progestin receptors. Five milligrams but not 0.5 mg RU 38486 inhibits the expression of sexual behavior in ovariectomized, estrogen-primed guinea pigs treated with 0.1 mg progesterone. This inhibition can be overcome by administration of a large dose of progesterone, suggesting that the drug-effect is specific to the progestin receptor system. RU 38486 binds, in vitro, to progestin receptors and decreases the availability of hypothalamic progestin receptors in estrogen-treated guinea pigs. These studies provide strong evidence that progesterone interaction with intracellular neural progestin receptors mediates the facilitation of sexual behavior by progesterone in female guinea pigs.

Animals↗
PubMed1984

The desensitization effect of progesterone on female rat sexual behavior is not due to interference with estrogen priming.

In order to determine if progesterone interferes with estradiol's priming action on progesterone-facilitated sexual behavior, we tested the responsiveness of progesterone-desensitized female rats to the serotonin receptor antagonist, methysergide, and the neuropeptide, luteinizing hormone-releasing hormone. Threshold doses of both compounds were established. Progesterone treatment, which caused a decrease in the lordosis rating in response to a moderate dose of progesterone did not inhibit responsiveness to threshold doses of methysergide or luteinizing hormone-releasing hormone. The results of this study support the notion that progesterone does not interfere with estradiol's priming action on progesterone-facilitated sexual receptivity. Furthermore, they suggest that progesterone's desensitization effect is specific to progesterone-facilitated lordosis.

Animals↗
PubMed1984

The relationship between heat abbreviation and neural progestin receptors in female rats.

The purpose of this study was to determine whether changes in the levels of neural progestin receptors are associated with mating-induced heat abbreviation in the rat. Mating caused a decrease, 8-10 hr after stimulation, in the duration of sexual receptivity. No difference in the concentration of cytosol progestin receptors was found between mated and nonmated animals 8-10 hr after treatment. Mating caused a statistically significant decrease in the concentration of nuclear progestin receptors at that time. However, this difference was probably not related to heat abbreviation, because no difference in nuclear progestin receptor levels was found between animals mated with vaginal masks and animals mated without masks, while mated-masked animals were found to exhibit significantly higher levels of sexual receptivity than mated-nonmasked animals after treatment. In addition, mating either with or without masks caused a statistically significant increase in serum progesterone levels relative to that measured in nonmated animals. Therefore, it is suggested that mating, even in the absence of cervical-vaginal stimulation, may cause the release of adrenal progestins which, in turn, may influence the rate at which neural progestin receptors accumulate and are processed within cell nuclei. The results of the present study suggest that mating-induced heat abbreviation in the rat is not associated with decreased levels of neural cytosol or nuclear progestin receptors.

Animals↗
PubMed1984

Supplemental progesterone delays heat termination and the loss of progestin receptors from hypothalamic cell nuclei in female guinea pigs.

Previous studies indicate that the retention of hypothalamic nuclear progestin receptors parallels the expression of sexual receptivity in ovariectomized, hormonally treated guinea pigs. In this study, the effect of a supplemental progesterone injection on heat termination and retention of nuclear progestin receptors was examined. Ovariectomized guinea pigs were injected with 50 micrograms progesterone 48 h after receiving 4 micrograms estradiol benzoate and were tested hourly for lordosis. 8 h after progesterone treatment, animals received either 500 micrograms progesterone or the oil vehicle. The supplemental progesterone injection delayed the termination of heat by more than 2 h compared to oil-injected animals. The effect of supplemental progesterone on the retention of nuclear progestin receptors was then determined. Animals were killed 8, 10, or 14 h after the initial injection of progesterone, and cytosol and nuclear progestin receptor concentrations in mediobasal hypothalamus-preoptic area were determined. Supplemental progesterone further increased the level of nuclear progestin receptors measured at 10 h, and at 14 h these levels were still elevated above baseline. In contrast, nuclear progestin receptor levels in animals which received only the initial progesterone injection had returned to baseline by 14 h, a time when similarly treated animals were no longer receptive. These results suggest that the mechanism by which heat termination occurs may involve loss of nuclear progestin receptors.

Animals↗