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J D Blaustein

Publications and source records attributed to J D Blaustein.

At least 37 records · Page 2Linked to original sources
PubMed1997

Leptin facilitates and inhibits sexual behavior in female hamsters.

Food deprivation decreases fertility in female mammals in part by inhibiting sexual behaviors. Genetically obese ob/ob mice, like food-deprived wild-type animals, are also infertile; treatment of ob/ob mice with leptin, the adipocyte-derived protein that they lack, corrects some of their reproductive deficiencies. We tested the hypothesis that leptin treatment would prevent the suppression of sexual receptivity that is caused by food deprivation in female Syrian hamsters. Instead, we found that treatment with murine leptin facilitated female sexual behavior in ad libitum-fed hamsters, but not in food-deprived animals. In food-deprived hamsters, leptin treatment actually intensified the inhibition of lordosis. Food deprivation decreased detectable estrogen receptor immunoreactivity (ERIR) in the ventromedial hypothalamus (VMH), but the leptin-induced changes in female sexual behavior were not accompanied by parallel changes in VMH ERIR. Thus leptin facilitates estrous behavior in hamsters, but it does not overcome the lordosis-inhibiting metabolic cues produced by acute food deprivation. Because circulating leptin levels are directly related to body fat content, an implication of these findings is that elevated levels of adipose tissue could have a positive influence on sexual responsiveness.

Analysis of Variance↗
PubMed1997

Convergence of substance P and estrogen receptor immunoreactivity in the midbrain central gray of female guinea pigs.

Substance P (SP) and estrogen receptor immunoreactivity overlap in the midbrain central gray (MCG) of female guinea pigs. Estrogen-receptor-containing cells are found throughout the rostrocaudal extent of the MCG. Moderately dense SP immunostaining is also found in this region. SP-immunoreactive punctate structures suggestive of boutons were found in close association with the processes of some estrogen-receptor-immunoreactive neurons. These associations were observed primarily in the lateral and ventrolateral MCG at the midcollicular and caudal levels. This findings suggests an anatomical substrate for interactions between SP and estradiol-sensitive neurons in the midbrain. Such interactions may underlie the effects of SP on female sexual behavior.

Animals↗
PubMed1997

Progesterone-independent activation of rat brain progestin receptors by reproductive stimuli.

Activation of steroid hormone receptors by steroid hormones alters both the physiology and behavior of animals. Steroid hormone receptors (e.g., progestin receptors) can also be activated in the absence of steroid hormones by pharmacological treatment with neurotransmitters or neuropeptides. However, it is not known if progesterone-independent activation of brain progestin receptors occurs under natural, physiological, conditions. We report that increases in reproductive behavior and brain immediate early gene expression in female rats induced by mating stimuli can be blocked by prior treatment with progesterone antagonists in the absence of circulating progesterone. This suggests that progestin receptors are activated in a progesterone-independent manner by a physiologically relevant stimulus in female rats, thus implicating a novel pathway by which mating stimuli and other environmental influences could activate steroid receptors to influence neuronal response and behavior.

Animals↗
PubMed1996

Reproductively-relevant stimuli induce Fos-immunoreactivity within progestin receptor-containing neurons in localized regions of female rat forebrain.

An experiment was conducted to determine if neurons that respond to stimuli associated with mating in female brain also contain progestin receptors. We found that a portion of the neurons that respond to stimuli associated with mating also contains progestin receptors. While the appropriate hormonal conditions are important for sexual receptivity, somatosensory information provided by the male also influences sexual behavior. One important stimulus provided by the male during copulation is vaginal-cervical stimulation (VCS). VCS has been shown to elicit many different behavioral and endocrine changes in female rats, such as increases in lordosis, pseudopregnancy, and termination of sexual receptivity. VCS also increases the expression of the immediate early gene product, Fos, in areas associated with reproduction. A portion of the neurons responding to VCS with increased Fos-immunoreactivity (Fos-IR) in female rat forebrain also contains estrogen receptors, illustrating that hormonal and mating-stimuli converge in a population of cells. As progesterone also plays an important role in female sex behavior, it is important to determine if some of the neurons also integrate information concerning serum progesterone levels and social interactions. Thus, we used a dual immunofluorescent technique to label both Fos-IR and progestin receptor-immunoreactivity (PR-IR) in the brains of estradiol-primed, ovariectomized female rats following VCS manually applied by the experimenter. Many of the neurons that respond to VCS with increased Fos-IR within the medial preoptic area, the arcuate nucleus, and the progestin receptor-rich areas of the rostral and caudal ventromedial nucleus of the hypothalamus also contain PR-IR.

Animals↗
PubMed1996

Effects of food deprivation on induction of neural progestin receptors by estradiol in Syrian hamsters.

Food deprivation, as well as treatment with metabolic inhibitors, suppress steroid hormone-induced estrous behavior in ovariectomized (OVX) Syrian hamsters. Previous work indicates that 48 h of food deprivation decreases the number of detectable estrogen receptor immunoreactive (ERIR) cells in the ventromedial hypothalamus (VMH) and the area just lateral to it (VLH), increases the number of ERIR cells in the medial preoptic area (MPO), and has no effect on the number of ERIR cells in the nucleus of the solitary tract in OVX hamsters. The present study examined the effects of food deprivation on neural progestin receptor binding using an in vitro binding assay and on progestin receptor immunoreactivity (PRIR) in estradiol-primed, OVX hamsters. Parallel behavior tests for sexual behavior were also performed in both experiments. OVX hamsters received 2.5 micrograms estradiol benzoate and were fed ad libitum or food deprived at the same time. Forty-eight hours later, animals were killed in preparation for the immunocytochemistry or progestin receptor assay. Binding assays indicated that 48-h food deprivation decreased progestin receptor levels in the preoptic area and had no effect in the mediobasal hypothalamus, an area that includes the VMH and the arcuate nucleus (ARH). Immunocytochemical analysis confirmed these findings. Food deprivation caused a decrease in sexual receptivity and in the number of detectable PRIR cells in the MPO and medial amygdala but had no effect on the number of detectable PRIR cells in the VMH/VLH, the ARH, or the anteroventral periventricular nucleus. These results suggest that food deprivation modulates progestin receptor binding and PRIR in a site-specific manner. In addition, the effects of food deprivation on neural ERIR and PRIR are significantly different.

Animals↗
PubMed1996

Dopamine requires the unoccupied progesterone receptor to induce sexual behavior in mice.

Using the recently generated mutant mice strain (PRKO) carrying a null mutation for the progesterone receptor (PR) gene by gene targeting, we examined the critical role of PR as a coordinator of key regulatory events involved in the steroid hormone and dopamine-facilitated sexual behavior in female mice. In vitro one-point binding analyses of estradiol benzoate (EB)-induced cellular PRs and immunohistochemistry of PR in the mediobasal hypothalamus demonstrated a reduction in binding in the homozygous females, equivalent to background levels seen in EB-unresponsive tissue. The biochemical findings correlated well with the behavioral observations, with the wild type females exhibiting high levels of lordosis, while the homozygous females showed minimal lordosis in response to mating by male mice. As a critical validation of our earlier studies on ligand-independent activation of PRs by dopamine, we examined the facilitation of sexual behavior by a dopamine agonist in the null mutants. Wild type females having the full complement of PRs exhibited high levels of lordosis, while the homozygous females showed minimal lordosis in response to dopamine. To determine whether this reduced response was due to a general lack of ability to express lordosis, mice were treated with another neurotransmitter, serotonin. No significant difference in the serotonin-facilitated lordosis response was observed between the wild type and the homozygous females. We conclude that multiple signal transduction pathways coexist in the neuroendocrine system for reproductive behavior, with PR acting as a transcriptional mediator for dopamine, as well as progesterone, to achieve integration of neural communication in the central nervous system.

Animals↗
PubMed1996

Efferent projections from the ovarian steroid receptor-containing area of the ventrolateral hypothalamus in female guinea pigs.

The ventrolateral hypothalamus (VLH) in female guinea pigs includes a subset of neurons which contain estrogen and progestin receptors, and which are implicated in the regulation of female sexual behavior by steroid hormones. However, little is known about where these neurons project, and consequently which other brain areas are involved in sexual behavior in female guinea pigs. The anterograde tracer Phaseolus vulgaris-Leucoagglutinin was used to label efferents from the ovarian steroid receptor-containing part of the VLH. To identify the correct placement of the tracer specifically within the group of neurons containing estrogen receptors, medial hypothalamic sections were also immunostained for estrogen receptors. Forebrain areas receiving dense projections from the ventrolateral hypothalamus included the bed nucleus of the stria terminalis, medial preoptic area, anterior hypothalamic area, anterior ventromedial hypothalamus, and caudal ventrolateral hypothalamus. The midbrain central gray was also heavily labeled. Moderate innervation was observed in the forebrain in the basolateral amygdala, medial preoptic nucleus, lateroanterior hypothalamic nucleus, dorsal hypothalamic areas, posterior hypothalamus, zona incerta, and in the midbrain interspersed among the central and lateral tegmental tracts. The major efferent pathways from the VLH appeared to travel rostrally through the mediobasal hypothalamus and preoptic area, and caudally via the medial thalamic nuclei and periventricular fiber system. These findings are similar to those of previous studies tracing the efferents from the ventromedial nucleus in rats and from the lateral hypothalamus in guinea pigs. Many of these areas that receive input from the steroid receptor rich area within the VLH are likely to be involved in the regulation of female sexual behavior.

Animals↗
PubMed1995

The suprachiasmatic area in the female hamster projects to neurons containing estrogen receptors and GnRH.

This study investigated whether the circadian regulation of luteinizing hormone (LH) release may be through direct input of the suprachiasmatic nucleus (SCN) to estrogen receptor (ER)- and/or gonadotropin releasing hormone (GnRH)-immunoreactive neurons. We used Phaseolus vulgaris leucoagglutinin (PHA-L) as an anterograde tracer of SCN efferents and performed double label immunocytochemistry for PHA-L and ER or GnRH. Between 8 and 30% of ER cells and 11-13% of the GnRH cells showed appositions with SCN efferents. Efferent projections of the subparaventricular hypothalamic nucleus and the retrochiasmatic area, relay stations of the circadian system, also made appositions with these two cell types. Results suggest that the circadian system could regulate the timing of the LH surge via two pathways, through input to GnRH and to ER cells.

Animals↗
PubMed1995

A subgroup of LHRH neurons in guinea pigs with progestin receptors is centrally positioned within the total population of LHRH neurons.

Although the role of gonadal steroids in inducing the LH surge is undisputed, the mechanism(s) whereby steroids induce the release of the hypothalamic luteinizing hormone-releasing hormone (LHRH) remain(s) enigmatic. In this study we examined the issue of the presence of steroid receptors in LHRH neurons using a mammalian species that has a true luteal phase, namely, guinea pigs. Progestin receptors (PR) were localized in LHRH neurons of ovariectomized guinea pigs administered estradiol (10-20 micrograms estradiol benzoate) for 3-4 days, using several different immunocytochemical protocols. The subgroup of LHRH neurons containing PR, although small, was strategically positioned within the core of the total population of LHRH neurons. This central position was visualized in simultaneous views of three-dimensional computer reconstructions of the populations of LHRH/PR neurons and LHRH neurons. The subgroup of LHRH/PR neurons formed a thread permeating the population of LHRH neurons. We propose that in guinea pigs, LHRH neurons containing progestin receptors, are foci of activity, capable of activating a larger component of the LHRH population of cells in certain endocrine conditions, such as prior to the LH surge.

Animals↗
PubMed1995

Progesterone enhances an estradiol-induced increase in Fos immunoreactivity in localized regions of female rat forebrain.

In female rats, the onset of reproductive behavior depends on the sequential presence of estradiol followed by progesterone. Although treatment with high doses of estradiol has been shown to increase immunostaining for the Fos protein, an immediate early gene product that is expressed upon cellular activation, another report conflicts with this finding. However, the previous reports agree that subsequent treatment with progesterone has no apparent effect on Fos expression. In order to resolve this discrepancy and investigate possible effects of progesterone, we used Fos immunocytochemistry combined with computer-aided image analysis. In experiment one, we found that treatment with 5 micrograms of estradiol increased Fos immunoreactivity (Fos-IR) within a section of the medial preoptic area and the dorsal medial hypothalamus. Subsequent treatment with 500 micrograms of progesterone 1 hr before perfusion increased the intensity of the immunostaining within the medial preoptic area and the dorsal medial hypothalamus, although it had no significant effect on Fos-IR cell number. In experiment 2, a lower concentration of Fos antiserum was used in order to diminish the immunostaining sensitivity to a level in which no increase of Fos-IR cell number was observed after treatment with estradiol. Under these immunocytochemical conditions, subsequent treatment with progesterone increased the number of Fos-IR cells in the medial preoptic area, the dorsal medial hypothalamus and the steroid receptor-rich area lateral to the ventromedial hypothalamus. Thus, treatment with behaviorally effective doses of both estradiol and progesterone induces Fos expression in localized regions of female rat brain.

Animals↗
PubMed1994

Convergent pathways for steroid hormone- and neurotransmitter-induced rat sexual behavior.

Estrogen and progesterone modulate gene expression in rodents by activation of intracellular receptors in the hypothalamus, which regulate neuronal networks that control female sexual behavior. However, the neurotransmitter dopamine has been shown to activate certain steroid receptors in a ligand-independent manner. A dopamine receptor stimulant and a D1 receptor agonist, but not a D2 receptor agonist, mimicked the effects of progesterone in facilitating sexual behavior in female rats. The facilitory effect of the neurotransmitter was blocked by progesterone receptor antagonists, a D1 receptor antagonist, or antisense oligonucleotides to the progesterone receptor. The results suggest that in rodents neurotransmitters may regulate in vivo gene expression and behavior by means of cross-talk with steroid receptors in the brain.

Adrenal Glands↗
PubMed1994

Estradiol and progesterone influence the response of ventromedial hypothalamic neurons to tactile stimuli associated with female reproduction.

Stimulation of the vagina and cervix, provided by the male during copulation or manually with a probe, causes many behavioral and endocrine changes associated with female reproduction in rats. Previously, we found that vaginal-cervical stimulation (VCS), by mating or manual probing, increases the expression of Fos-immunoreactivity (Fos-IR) in discrete populations of neurons in the preoptic area, mediobasal hypothalamus and midbrain, suggesting that these neurons respond to VCS. The purpose of the present study was to determine if hormonal priming would increase the number of Fos-IR cells following VCS. Contrary to our hypothesis, in Experiment 1 priming animals with a behaviorally effective dose of 17 beta-estradiol benzoate followed 48 h later by progesterone caused a trend towards a decrease in the number of VCS-induced Fos-IR cells in the ventromedial hypothalamus. In Experiment 2, which was done to confirm this decrease in VCS-induced Fos-IR neurons by hormones, this effect was found to be statistically significant. Furthermore, this hormone-induced decrease in VCS-responsive cells was localized to the ventromedial nucleus of the hypothalamus, an area rich in estrogen and progestin receptors. No effects of hormone treatment on VCS-induced Fos-IR were observed in any other brain regions analyzed. These findings suggest that steroid hormones may elicit some of their effects on female reproductive behavior and physiology by altering the responsiveness of ventromedial nucleus neurons to vaginal-cervical stimulation.

Animals↗
PubMed1994

Hypothalamic ovarian steroid hormone-sensitive neurons involved in female sexual behavior.

Estradiol and progesterone regulate sexual behaviors in guinea pigs and rats, at least in part, through interaction with intracellular steroid hormone receptors. In the present review of work from the laboratory of the authors, we summarize recent work which has focused on one of the sites of hormone action in female guinea pigs--the ventrolateral hypothalamus. We summarize results of earlier experiments in which the regulation of steroid hormone receptors in this area was assessed after hormonal treatments with predictable effects on female sexual behavior. We then review the results of recent tract-tracing experiments in which we have examined the projections from the steroid receptor-immunoreactive neurons in this region, as well as the afferent projections from other neuroanatomical areas, including neurons which themselves contain estrogen receptors. We also present studies on the afferent input into these neurons by noradrenergic neurons and discuss the possibility that noradrenergic input influences steroid hormone sensitivity in these neurons. Finally, we discuss the results of experiments in which Fos-immunocytochemistry was used in rats to identify the neurons responding to a particular tactile stimulus associated with female reproduction, i.e., vaginal-cervical stimulation. These experiments further define a complex neuroanatomical system, in which many of the elements are estradiol or progesterone-responsive, that is involved in the hormonal regulation of sexual behavior in guinea pigs and rats.

Afferent Pathways↗
PubMed1994

Projections from ventrolateral hypothalamic neurons containing progestin receptor- and substance P-immunoreactivity to specific forebrain and midbrain areas in female guinea pigs.

Many neurons within the ventrolateral hypothalamus in guinea pigs contain estrogen-induced progestin receptors as well as substance P. Retrograde tracing combined with immunocytochemistry was used to determine the specific projections of this subset of steroid-sensitive cells. Unilateral Fluoro-Gold injections into the dorsal midbrain, including the central gray, labeled a large proportion of the ventrolateral hypothalamic neurons immunoreactive for both progestin receptors and substance P (approximately 30%); substantially fewer of these neurons were labeled by unilateral Fluoro-Gold injections into the preoptic area (approximately 6%), medial amygdala (approximately 10%), or the bed nucleus of the stria terminalis (approximately 11%). The projections of progestin receptor-immunoreactive neurons in the ventrolateral hypothalamus were similar to those of progestin receptor/substance P double-labeled neurons, while a slightly lower percentage of the ventrolateral hypothalamic, substance P-immunoreactive neurons tended to project to each of these areas. These pathways may prove to be components of the neural circuitry underlying a variety of functions influenced by gonadal steroid hormones and substance P, such as female sexual behavior, salt intake, nociception and aggression.

Amygdala↗
PubMed1994

Intraneuronal convergence of tactile and hormonal stimuli associated with female reproduction in rats.

Stimulation of the vagina and cervix, by mating or manual probing, elicits many behavioral and endocrine changes associated with female reproduction in rats. We and others have identified neurons in the medial preoptic area, medial division of the bed nucleus of the stria terminalis, posterodorsal portion of the medial amygdala, ventromedial hypothalamus, dorsomedial hypothalamus and midbrain central gray that increase Fos expression in response to vaginal-cervical stimulation (VCS). In the present study, we used a double-label immunofluorescent technique to determine if any of these VCS-responsive neurons also contained estrogen receptor-immunoreactivity. We found that over 80% of the VCS-induced Fos-IR neurons in the medial division of the bed nucleus of the stria terminalis also contained estrogen receptor-immunoreactivity. Furthermore, high percentages of VCS-responsive neurons in the medial preoptic area, posterodorsal medial amygdala, ventromedial hypothalamus and midbrain central gray contained estrogen receptor-immunoreactivity as well. These results suggest that sensory and hormonal information associated with female reproduction converge on specific populations of neurons and may be integrated at the molecular level within these neurons.

Animals↗
PubMed1994

Down-regulation of estrogen receptor immunoreactivity by 17 beta-estradiol in the guinea pig forebrain.

Low amplitude pulses of estradiol-17 beta (E2-17 beta) are more effective than large single bolus injections or constant exposure to E2-17 beta in inducing progesterone-facilitated sex behavior in female rats and guinea pigs. The present study examined whether the increased responsiveness to E2-17 beta is due to an increase in the number of estrogen receptors in the estrogen receptor rich areas of the hypothalamus and amygdala. Initial studies examined the rapid effects (20 min) of a high dose of E2-17 beta (50 micrograms) on estrogen receptor immunostaining using either the H222 antibody or the ER 21 antiserum. ER 21 immunostaining was not affected by the E2-17 beta treatment suggesting that it binds to both occupied and unoccupied estrogen receptors. Therefore the ER 21 antiserum was used to characterize the regulation of estrogen receptor immunoreactivity (ER-IR) by E2-17 beta. ER-IR was examined for 48 h and serum E2-17 beta for 24 h following a 2 micrograms s.c. injection of E2-17 beta (a dose similar to that used in multiple pulse paradigms). Serum E2-17 beta peaked 15 to 30 min following the injection and returned to baseline values by 1 h. In all but one area maximal suppression of ER-IR occurred at 12 h. In summary, 1) decreases in estrogen receptor immunoreactivity following E2-17 beta are consistent with studies in which estrogen receptors were assayed by binding assays and estrogen receptor mRNA was determined by in situ hybridization; 2) the ER 21 antiserum is able to detect both occupied and unoccupied estrogen receptors and 3) H222 immunoreactivity is influenced by the presence of E2-17 beta, so that the level of H222-IR is a reflection of ligand/receptor binding dynamics. The data suggest that up-regulation of estrogen receptors does not account for the increase in behavioral sensitivity which is observed following multiple pulses of E2-17 beta.

Amygdala↗
PubMed1994

Distribution of androgen receptor immunoreactivity in vasopressin- and oxytocin-immunoreactive neurons in the male rat brain.

Arginine vasopressin-immunoreactive (AVP-ir) neurons in the bed nucleus of stria terminalis (BST) and medial amygdaloid nucleus are very responsive to gonadal hormones. After gonadectomy, these neurons lose their AVP immunoreactivity and stop expressing AVP mRNA. Testosterone treatment reverses these changes, acting via androgen as well as estrogen receptor-mediated mechanisms. Although AVP-ir neurons contain estrogen receptor immunoreactivity, it is not known whether they also contain androgen receptor immunoreactivity. To answer this question, brains of male rats were stained immunocytochemically for AVP as well as for androgen receptors. In the BST and medial amygdaloid nucleus, respectively, 90.5% and 91.2% of the AVP-ir neurons contained androgen receptor immunoreactivity. In contrast, in the suprachiasmatic nucleus, the supraoptic nucleus, and the magnocellular portion of the paraventricular nucleus (PVN), none of the AVP-ir neurons contained androgen receptor immunoreactivity. In the ventral zone of the medial parvocellular part of the PVN (mpvPVN), 4.3% of the scattered AVP-ir neurons contained androgen receptor immunoreactivity. One of the control experiments, i.e. staining sections for oxytocin (OT) rather than AVP, revealed that although OT-ir neurons in the supraoptic and magnocellular portion of the PVN did not contain androgen receptor immunoreactivity, 52.5% of the OT-ir neurons in the mpvPVN did. The results suggest that androgens can bind to androgen receptors in AVP-ir neurons in the BST and medial amygdaloid nucleus, possibly to influence AVP expression. The results also suggest that androgens can bind to androgen receptors in AVP-ir and OT-ir neurons in the mpvPVN. The function of the latter interaction, however, is unclear.

Animals↗