Biomedical subjects

J D Blaustein

Publications and source records attributed to J D Blaustein.

At least 55 records · Page 3Linked to original sources

PubMed1994

Manipulations of metabolic fuel availability alter estrous behavior and neural estrogen receptor immunoreactivity in Syrian hamsters.

Decreases in metabolic fuel utilization caused by food deprivation, diabetes, or treatment with metabolic inhibitors have been shown to suppress steroid-induced estrous behavior in ovariectomized Syrian hamsters. These same manipulations also caused a decrease in the number of detectable estrogen-receptor immunoreactive (ERIR) cells in the ventromedial hypothalamus (VMH) and the adjacent area lateral to it (VLH) in ovariectomized hamsters. Forty-eight hours of food deprivation or treatment with pharmacological blockers of glycolysis (2-deoxy-D-glucose) and fatty acid oxidation (methyl palmoxirate) decreased the number of detectable ERIR cells in the VMH/VLH. However, neither inhibitor given alone was sufficient to affect the number of detectable ERIR cells in the VMH/VLH, even when given in much higher doses. Therefore, the number of ERIR cells in the VMH/VLH, like steroid-induced estrous behavior, responds only to a combination of glucoprivation and lipoprivation and not to either alone. The effects of metabolic fuel restriction are not due to a general suppression of neural ERIR, because food deprivation or treatment with 2-deoxy-D-glucose and methyl palmoxirate actually increased the number of detectable ERIR cells in the medial preoptic area (mPOA) and had no effect in the nucleus of the solitary tract. Lesions destroying the area postrema (AP) prevented the decrease in ERIR cells in the VMH/VLH and the inhibition of estrous behavior caused by fuel restriction. However, AP lesions did not alter the effects of metabolic inhibitors on ERIR in the mPOA. On the other hand, subdiaphragmatic vagotomy abolished the effects of metabolic inhibitors on mPOA ERIR, but did not affect either lordosis or VMH/VLH ERIR. These results suggest that the suppression of estrous behavior induced by metabolic fuel restriction is at least in part due to a decrease in the number of ERIR neurons in the VMH/VLH. In addition, the estrogen-sensitive neurons in the VMH/VLH and mPOA receive metabolic cues via different neural pathways. The AP, but not vagus nerves, is required for ERIR neurons in the VMH/VLH to detect fuel availability; the vagus nerves, but not the AP, are necessary for estrogen-binding neurons in the mPOA to detect visceral information.

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PubMed1994

Inhibition of rat sexual behavior by antisense oligonucleotides to the progesterone receptor.

To test further the idea that sexual behavior in rodents is mediated via the progesterone receptor (PR) in the ventromedial nucleus of the hypothalamus, antisense and sense oligonucleotides to progesterone receptor were administered intracerebroventricularly into the third cerebral ventricle of ovariectomized estrogen-primed animals. Progesterone-facilitated sexual behavior was inhibited in animals treated with antisense oligonucleotides, with proceptive and receptive responses being minimal or completely suppressed. Sexual behavior was not altered by control sense oligonucleotides. In vitro binding assays of the cytosol progesterone receptors demonstrated a 52.2% reduction of PRs in the hypothalamus of animals that received antisense oligonucleotides, suggesting a reduction in PR synthesis. These data suggest that a threshold level of estrogen-induced hypothalamic PR is critical in the regulation of progesterone-facilitated sexual behavior in female rats.

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PubMed1993

Estrogen-receptor immunoreactivity in hamster brain: preoptic area, hypothalamus and amygdala.

The distribution of estrogen-receptor containing cells in the preoptic area, hypothalamus and amygdala of female Syrian hamster brain was studied by immunocytochemical methods. Dense populations of estrogen-receptor immunoreactive (ER-IR) cells were found in the medial preoptic area, the bed nucleus of the stria terminalis, amygdala, ventral and lateral parts of the hypothalamus, and the arcuate nucleus. Injection of estradiol caused a decrease in estrogen-receptor immunoreactivity (ERIR) containing cells within one hour, a decrease that may reflect a change in the ability of the occupied estrogen receptor to bind the particular antibody (H222) used rather than down-regulation of the estrogen receptor. Our findings on the distribution of estrogen-receptor containing cells in these areas using an immunocytochemical technique are consistent with and extend the findings of others using autoradiographic and in vitro binding techniques to study estrogen receptor distribution in hamster brain.

Amygdala↗

PubMed1993

Estrogen receptor-immunoreactive forebrain neurons project to the ventrolateral hypothalamus in female guinea pigs.

In rodents, the facilitation of sexual receptivity by estradiol and progesterone is suspected to be mediated by a network of neurons containing estrogen and progestin receptors. In female guinea pigs, this network would include estrogen receptor-immunoreactive (ER-ir) neurons located within the rostro-ventral ventrolateral hypothalamus (r-vVLH). This hypothesis predicts that a proportion of the neurons projecting to the r-vVLH contains estrogen receptors. This prediction was tested through retrograde tracing combined with immunocytochemistry for estrogen receptors. Retrogradely labelled neurons were particularly abundant within the medial preoptic nucleus (MPN), bed nucleus of the stria terminalis (BST), anterior hypothalamus, amygdala, and lateral parabrachial nucleus. As predicted by the hypothesis, retrogradely labelled neurons were mostly observed in estrogen receptor-rich areas. Retrogradely labelled neurons also containing estrogen receptor-immunoreactivity (ER-IR) were primarily found within the MPN, BST, and amygdala. However, a majority of retrogradely labelled neurons did not contain ER-IR. As the preoptic area and the r-vVLH are both responsive to estradiol in the facilitation of sexual receptivity by progesterone, these data are consistent with the hypothesis tested. However, our data also suggest that the network of neurons controlling sexual receptivity may include elements not directly sensitive to estradiol. Finally, the location of retrogradely labelled neurons is discussed with respect to the stimuli provided to the r-vVLH in the context of sexual receptivity facilitated by estradiol and progesterone.

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PubMed1993

Immunocytochemical localization of midbrain estrogen receptor- and progestin receptor-containing cells in female guinea pigs.

In the guinea pig midbrain, a low concentration of progestin receptors is induced by estradiol. This is in contrast to the mediobasal hypothalamus which has a large number of estradiol-induced progestin receptors. Because the midbrain is an important site for the hormonal regulation of sexual behavior, we mapped the distribution of cells containing estrogen receptor- and estradiol-induced progestin receptor-immunoreactivity in that area. Estrogen receptor-immunoreactive cells are found in midbrain sites previously reported, including the midbrain central gray, the tegmentum lateral and ventral to the central gray, peripeduncular region, and parabrachial nuclei. While progestin receptor-immunoreactive cells were not detected without estradiol priming, estradiol-induced progestin receptors were found throughout the rostrocaudal extent of the midbrain central gray and adjacent tegmental area. Progestin receptor-immunoreactive cells were far fewer than estrogen receptor containing cells, had less cytoplasmic staining, and appeared restricted to the midbrain central gray, lateral and ventrolateral to the cerebral aqueduct and the adjacent tegmental area.

Animals↗

PubMed1993

Colchicine-induced accumulation of estrogen receptor and progestin receptor immunoreactivity in atypical areas in guinea-pig brain.

Using immunocytochemical techniques, cells containing estrogen and progestin receptors have been observed in many discrete regions of the guinea-pig forebrain, including the mediobasal hypothalamus and preoptic area. While most reaction product is located within cell nuclei, we have reported abundant reaction product in perikaryal cytoplasm and neuronal processes as well. Ultrastructural analysis has revealed the presence of estrogen and progestin receptors in atypical subcellular sites within the hypothalamus, including dendrites and axon terminals. In order to determine if microtubule-dependent intracellular transport is involved in intraneuronal transport of steroid hormone receptors, ovariectomized guinea-pigs were injected intracerebroventricularly with the microtubule inhibitor, colchicine, and brain sections at the level of the hypothalamus were immunostained for estrogen receptors. This treatment resulted in the appearance of estrogen receptor immunoreactivity in the paraventricular and mediodorsal thalamic region, areas typically devoid of estrogen receptor-immunoreactive cells in guinea-pigs. In a second study on progestin receptors, we observed the colchicine-induced accumulation of progestin receptor immunoreactivity in the paraventricular thalamic, mediodorsal thalamic and lateral dorsal thalamic areas as well as in the medial amygdala, all areas typically devoid of progestin receptor immunoreactivity. While estradiol injection induced progestin receptor immunoreactivity in the hypothalamus and preoptic area as described previously, it had no effect on the colchicine-induced accumulation in the thalamus and amygdala. These results provide evidence that in some neurons, progestin receptors and estrogen receptors are transported intracellularly, apparently at a rapid enough rate that they do not ordinarily accumulate within the perikaryon.

Amygdala↗

PubMed1993

Fos expression in the rat brain following vaginal-cervical stimulation by mating and manual probing.

Vaginal-cervical stimulation (VCS), provided by mating or manual probing, induces many reproductive behavioral and endocrine changes in female rats. These changes include an increase in lordosis duration, heat termination and pseudopregnancy. Electrophysiological and [14C]2-deoxy-D-glucose studies collectively show that neurons in the medial preoptic area, ventromedial hypothalamus and midbrain central gray respond to manual VCS. In the present study we immunocytochemically labeled brain sections for Fos, the protein product of the immediate early gene c-fos, to detect VCS-responsive neurons in hormone-primed animals receiving VCS by mating or manual probing. In Experiment 1, females receiving mounts and intromissions were compared to: 1) vaginally-masked females receiving mounts but no VCS, 2) females exposed to an intact anesthetized male or 3) females not exposed to males or the testing arena. Those animals receiving VCS showed a dramatic increase in the number of Fos-immunoreactive cells in the medial preoptic area, posterodorsal portion of the medial amygdala and bed nucleus of the stria terminalis, as well as the dorsomedial hypothalamus, ventromedial hypothalamus and midbrain central gray. These effects of VCS were confirmed in Experiment 2 in animals receiving manual vaginal-cervical probing. These findings extend previous electrophysiological and [14C]2-deoxy-D-glucose studies by providing evidence that additional brain areas respond to VCS by mating, as well as manual probing.

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PubMed1993

ICI 182,780: a pure antiestrogen that affects behaviors and energy balance in rats without acting in the brain.

ICI 182,780 is one of a new class of steroidal antiestrogens that differs from nonsteroidal antiestrogens, such as tamoxifen, in a number of respects. 1) It is bound by estrogen receptors with a high affinity, similar to that for estradiol. 2) It is a "pure" antiestrogen in that it does not mimic any of the effects of estradiol. 3) This class of antiestrogens does not seem to be bound by antiestrogen binding sites. 4) ICI 182,780 may not be active in the brain after peripheral administration. Indeed, ICI 182,780 blocked in vivo cell nuclear binding of [3H]estradiol in uterus, pituitary, and adipose tissue but not in hypothalamus-preoptic area. In vitro, ICI 182,780 competed for binding by neural estrogen receptors with an affinity comparable with that for estradiol. When given to ovariectomized rats, ICI 182,780 did not mimic any of the actions of estradiol. Instead, ICI 182,780 treatment completely blocked the uterotrophic effects of estradiol and attenuated the actions of estradiol on linear growth, carcass fat content, fat pad weight, and sexual receptivity. Treatment with ICI 182,780 also attenuated the estrogenic effects of tamoxifen on food intake, body weight and composition, linear growth, and uterine weight. These findings support the concept that, in addition to its actions in the brain, estradiol can act peripherally to modulate regulatory behaviors, energy balance, and estrous behavior. They are also consistent with the hypothesis that nonsteroidal antiestrogens, such as tamoxifen, affect energy balance via estrogen receptors, rather than antiestrogen binding sites.

Animals↗

PubMed1993

ICI 182,780 antagonizes the effects of estradiol on estrous behavior and energy balance in Syrian hamsters.

Three experiments examined the effects of ICI 182,780, a steroidal "pure" antiestrogen that is thought to be active peripherally but not in the brain when given systemically, on energy balance, estrous behavior, and in vivo cell nuclear binding of [3H]estradiol in Syrian hamsters. Pretreatment with ICI 182,780 reduced in vivo uptake of [3H]estradiol in uterus but not in pooled hypothalamus-preoptic area. Ovariectomized Syrian hamsters were treated with estradiol benzoate (EB, 5 micrograms/day), ICI 182,780 (250 micrograms/day), or both EB and ICI 182,780 for 4 wk. Estradiol treatment caused significant decreases in food intake, body weight and fat content, and linear growth. Given alone, ICI 182,780 had no effect on these measures. When they were given concurrently, ICI 182,780 attenuated the effects of estradiol on body weight, growth, and fat content but not on food intake. Treatment with ICI 182,780 significantly diminished estrous behavior induced with either EB plus progesterone or with EB alone. These findings support the hypothesis that, in addition to its actions in the brain, estradiol acts peripherally to modulate estrous behavior and energy balance.

Animals↗

PubMed1993

Estrogen receptor immunoreactivity in rat brain: rapid effects of estradiol injection.

The existence of cytoplasmic estrogen receptor immunoreactivity (ER-IR) has been reported in the brain using three different antibodies raised against different epitopes on the ER protein. With each antibody, the darkest reaction product was seen within cell nuclei, but cytoplasmic ER-IR was also observed with each antibody in most neuroanatomical areas. We have reported previously that an injection of estradiol causes a rapid decrease in ER-IR in ovariectomized guinea pigs when the H 222 estrogen receptor antibody was used. In extending this work to rats, we used three different ER antibodies to determine if this decrease in ER-IR is likely to be due to down-regulation of the receptor by estradiol or a decrease in the ability of some antibodies to bind to their particular epitopes on the receptor. Estradiol injection in ovariectomized rats caused a rapid (within 20 min), nearly total loss of cytoplasmic ER-IR when the H 222 antibody was used to visualize the receptor. This decrease did not appear to be due to movement of the receptors to the cell nucleus, as cell nuclear ER-IR also decreased. When other antibodies were used, the extent of loss and the pattern of immunostaining were greatly influenced by the particular antibody. Extensive loss of cytoplasmic and cell nuclear ER-IR was seen when an antiserum against the hinge region of the receptor was used. However, when an antiserum against the N-terminus of the ER was used, a decrease was seen in cytoplasmic ER-IR, but little or no decrease was observed in cell nuclear ER-IR. Because loss of cell nuclear ER-IR was not seen with all of the antibodies, these results suggest that the dramatic decrease in cell nuclear ER-IR seen immediately after estradiol injection is due at least in part to a conformational change in the receptor. This, in turn, may impede association with particular antibodies during the immunocytochemical procedure.

Amygdala↗

PubMed1992

Neural distribution of estrogen receptor immunoreactive cells in the female musk shrew.

In this report we describe the neural distribution of estrogen receptor immunoreactivity (ER-IR) in the female musk shrew (Suncus murinus). The highest concentrations of neurons containing ER-IR were found in the preoptic areas, the lateral septum, the anterior arcuate and ventromedial nuclei of the hypothalamus, the medial nuclei of amygdala, and the midbrain central grey. Additional preoptic, hypothalamic, limbic and midbrain nuclei also contained ER-IR cells. The distribution of ER-IR was similar to that described in other mammals and birds, with several important differences. In the female musk shrew, there was little difference in ER-IR intensity or distribution when brains from gonadally intact and ovariectomized musk shrews were compared. In addition, long-term treatment with a supraphysiological dose of estradiol was required to detect a decrease in ER-IR intensity. Finally ER-IR was noted in both nuclear and cytoplasmic regions of cells in ovariectomized and gonadally intact musk shrews. The dense ER-IR noted in intact females as well as the presence of cytoplasmic stain may be due to the unusual relationship between estradiol, ovulation and sexual receptivity in this species.

Animals↗

PubMed1992

Estradiol pulses induce progestin receptors selectively in substance P-immunoreactive neurons in the ventrolateral hypothalamus of female guinea pigs.

Low doses of estradiol, administered as pulses, are as effective as higher doses for priming ovariectomized (OVX) guinea pigs to display progesterone-facilitated lordosis. High doses of estradiol, administered by constant-release implants, induce progestin receptors in many substance P-immunoreactive (SP-IR) neurons in the ventrolateral hypothalamus (VLH), a site at which estradiol primes OVX guinea pigs to respond behaviorally to progesterone. To test the hypothesis that behaviorally effective estradiol pulses induce progestin receptors selectively in substance P-containing neurons in the VLH, OVX females received estradiol implants 1 week prior to perfusion, or two pulses of estradiol-17 beta, injected 39 and 11 h before perfusion. Colchicine was administered intracerebroventricularly prior to perfusion. No significant differences were observed in the total number of progestin receptor-immunoreactive (PR-IR) or substance P-immunoreactive cells in the VLH and VLH/ventromedial hypothalamus (VMH), respectively, of females receiving the two estradiol treatments. However, the percentage of PR-IR cells in the VLH also immunoreactive for SP was significantly higher in the estradiol pulse-treated (53%), than in the estradiol capsule-implanted animals (36%). These data suggest that behaviorally effective estradiol pulses induce progestin receptors selectively in substance P-containing neurons in the VLH and are consistent with the hypothesis that substance P is involved in progesterone-facilitated lordosis in guinea pigs.

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PubMed1992

Progestin receptors in substance P-immunoreactive neurons in the hypothalamus of male guinea pigs after behaviorally effective estradiol pulse treatment.

Pulsatile administration of estradiol effectively primes orchidectomized (ORCH) male guinea pigs to display progesterone-facilitated lordosis. In contrast, a single injection of estradiol benzoate (EB) is not behaviorally effective. In ovariectomized female guinea pigs, estradiol pulses induce progestin receptors selectively in substance P neurons in the ventrolateral hypothalamus (VLH), a site at which estradiol primes females to respond behaviorally to progesterone. To test the hypothesis that behaviorally effective estradiol pulses induce progestin receptors selectively in substance P neurons in the VLH in males, ORCH animals received a single injection of EB 40 h before, or two pulses of estradiol-17 beta, 39 and 11 h before perfusion. Colchicine was administered intracerebroventricularly prior to perfusion. The only difference found between the two estradiol treatment groups was a higher number of progestin receptor-immunoreactive (PR-IR) cells in the rostral VLH of estradiol pulse-treated males. There were no significant differences in the number of PR-IR cells in the mid- or caudal VLH, nor in the number of substance P-immunoreactive (SP-IR) neurons in the VLH/ventromedial hypothalamus (VMH) of animals receiving the two estradiol treatments. Furthermore, the percentage of PR-IR cells in the VLH also immunoreactive for SP did not differ between the estradiol pulse- (22%-25%) and the EB-injected animals (22%-32%). These data do not support the hypothesis that administration of behaviorally effective estradiol pulses, as compared to behaviorally ineffective EB injections, induce progestin receptors selectively in substance P neurons in the VLH of male guinea pigs.

Animals↗

PubMed1992

Estrogen receptors in dendrites and axon terminals in the guinea pig hypothalamus.

The ultrastructural localization of steroid hormone receptors has been made possible by the development of immunocytochemical procedures using monoclonal antibodies. Estrogen receptor-immunoreactivity (ER-IR) in the brain is present most abundantly in neuronal nuclei when observed with light microscopy. However, we have also observed ER-IR in the perikarya and cytoplasmic processes of neurons. To determine the organelles with which the cytoplasmic ER-IR is associated, we developed a technique for ultrastructural visualization of ER-IR. Ovariectomized guinea pigs were perfused, brains vibratome-sectioned, and estrogen receptors immunostained by either an immunoperoxidase-diaminobenzidine technique or by an immunogold-streptavidin procedure, each followed by silver intensification. Electron microscopic analysis confirmed distribution of ER-IR throughout cell nuclei, but ER-IR was also observed in proximal and distal dendrites and rough endoplasmic reticulum. Most surprisingly, however, ER-IR was found in many axon terminals containing predominantly round, and in some cases, flattened clear synaptic vesicles. Parallel experiments examining the distribution of progestin receptors confirmed the localization at the same subcellular sites as for estrogen receptors. The results of this experiment corroborate our earlier findings of extranuclear steroid receptor-immunoreactivity in the brain, and they suggest potential nongenomic sites of action for estradiol and progesterone in dendrites and axon terminals.

Animals↗

PubMed1992

Cytoplasmic estrogen receptors in rat brain: immunocytochemical evidence using three antibodies with distinct epitopes.

The existence of cytoplasmic estrogen receptors (ERs) has been reported in the guinea pig brain using immunocytochemical techniques. While cytoplasmic ERs have been reported recently in other species, such as opossum, musk shrew, and ferrets, an exclusively cell nuclear pattern of ER immunoreactivity has been reported in the rat brain. Because all studies that have reported the existence of cytoplasmic ERs in the brain have used the H 222 monoclonal antibody, the possibility exists that this observation is idiosyncratic to this antibody. In the present experiment three antibodies directed against diverse epitopes on the ER protein were used to immunocytochemically stain ERs in rat brain. With each antibody, ER immunoreactivity was observed in the hypothalamus, preoptic area, amygdala, and midbrain periaqueductal gray. In all cases we observed the highest density of reaction product in cell nuclei, but extensive cytoplasmic immunostaining was observed in most areas as well. In addition to demonstrating the existence of neural ER immunoreactivity in perikaryal cytoplasm and cytoplasmic processes in the brain, this study suggests that the neural cytoplasmic ER immunoreactivity is not just a small fragment of the receptor protein; rather, it is likely to be the entire receptor.

Animals↗

PubMed1992

Expression of Fos-like proteins in gonadotropin-releasing hormone neurons of Syrian hamsters: effects of estrous cycles and metabolic fuels.

In female mammals, reproduction is sensitive to the availability of metabolic fuels, and food deprivation has been shown to suppress pulsatile LH secretion, attenuate the preovulatory LH surge, and prevent ovulation. It has been suggested that food deprivation impairs fertility by reducing the secretion of GnRH by GnRH-producing neurons in the forebrain. A series of experiments tested this hypothesis by examining the effects of estrous cycles and manipulations of metabolic fuel availability on the expression of Fos-like proteins (Fos-IR) in GnRH-immunoreactive (GnRH-IR) neurons in the forebrain of Syrian hamsters. GnRH-IR neurons were detected in several areas, including the diagonal band of Broca (DBB), medial septum (MS), rostral medial preoptic area (mPOA), and caudal POA. In the more rostral regions (DBB and MS/mPOA), GnRH-IR neurons expressed Fos-IR almost exclusively on day 4 of the cycle, just after the preovulatory LH surge. However, in the caudal POA, GnRH-IR neurons expressed Fos-IR across the entire cycle, including days 1-3, when LH secretion is pulsatile. Food deprivation on days 1 and 2 of the cycle, which attenuates the LH surge and blocks ovulation in hamsters, significantly reduced the proportion of GnRH-IR neurons that expressed Fos-IR on days 2 and 4 (caudal POA) or only on day 4 (DBB and MS/mPOA). Suppression of fuel availability with insulin or 2-deoxy-D-glucose on day 1 of the cycle mimicked the effects of food deprivation and reduced the proportion of caudal POA GnRH-IR neurons that expressed Fos-IR. The results of these experiments suggest that in Syrian hamsters, there are separate populations of GnRH-IR neurons associated with pulsatile and surge modes of LH secretion. In addition, the fact that manipulations of metabolic fuel availability cause changes in the expression of Fos-IR in both populations of GnRH-IR neurons provides strong support for the hypothesis that nutritional infertility is due in part to decreased GnRH secretion.

Animals↗

PubMed1991

Immunocytochemical evidence for noradrenergic regulation of estrogen receptor concentrations in the guinea pig hypothalamus.

The noradrenergic system interacts with steroid hormones to influence female sexual behavior and gonadotropin release in rodents. Using a double label immunocytochemical procedure for estrogen receptors and dopamine-beta-hydroxylase, we investigated the anatomical relationships between noradrenergic neurons and estrogen receptor-immunoreactive (ER-IR) cells in the brain of ovariectomized female guinea pigs. Dopamine-beta-hydroxylase-immunoreactive (DBH-IR) varicosities were closely associated with ER-IR cells throughout the hypothalamus and preoptic area. This anatomical relationship was observed with almost 80% of the ER-IR cells in the ventrolateral hypothalamus (VLH), an area involved in the regulation of female sexual behavior in guinea pigs. Furthermore, the presence of closely associated DBH-IR varicosities was related to staining intensity of ER-IR neurons. In the rostral VLH, ER-IR neurons with closely associated DBH-IR varicosities stained more darkly than ER-IR neurons lacking this association, suggesting noradrenergic regulation of basal levels of cellular estrogen receptors. These findings provide neuroanatomical evidence suggestive of noradrenergic regulation of estrogen receptor levels in the hypothalamus of female guinea pigs.

Animals↗

PubMed1991

A site for estradiol priming of progesterone-facilitated sexual receptivity in the ventrolateral hypothalamus of female guinea pigs.

The induction of progestin receptors by estradiol in the mediobasal hypothalamus (MBH) has been correlated with progesterone facilitation of sexual receptivity in female guinea pigs. We used an immunocytochemical technique to visualize the induction of progestin receptors by estradiol in a population of neurons correlated with estradiol-induced responsiveness to progesterone. Progestin receptor-immunoreactivity (PR-IR) and responsiveness to progesterone-facilitation of sexual behavior were induced by intracranial implantation of small bilateral cannulae (28- or 33-gauge) containing 1 or 10% estradiol diluted with cholesterol. In the first experiment, 28-gauge cannulae containing estradiol were effective only when implanted in the rostral part of the MBH. In the second experiment in which 33-gauge cannulae were used, behavioral responsiveness to progesterone was induced only when the cannulae were localized bilaterally in the rostro-ventral part of the ventrolateral hypothalamus (VLH). The presence of estradiol-induced PR-IR within the rostro-ventral VLH was correlated with the ability of progesterone to facilitate sexual behavior. These data suggest that neurons containing estrogen-induced progestin receptors specifically within the rostro-ventral VLH are involved in progesterone facilitation of sexual receptivity in estradiol-primed guinea pigs.

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