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Estradiol control of expression and levels of estradiol-binding proteins in the medial preoptic area, medial hypothalamus and pituitary.

The brains of mammals have at least three estradiol-binding proteins: estradiol receptor-alpha (ERalpha), ERbeta, and sex hormone-binding globulin (SHBG). In this study we compare the effects of estradiol treatment on the expression of mRNA for these three estradiol-binding proteins in two reproductively important brain areas, the medial preoptic area-anterior hypothalamus (MPOA-AH) and medial hypothalamus (MH) as well as in the hippocampus in ovariectomized rats, using the reverse transcriptase-polymerase chain reaction (RT-PCR). We also used surface-enhanced laser desorption ionization time of flight (SELDI-TOF) mass spectrometry (MS) to analyze the effects of estradiol in ovariectomized rats on SHBG levels in the MPOA-MH as well as the neurohypophysis. In vivo estradiol treatment in ovariectomized rats eliminated or significantly reduced expression of all three estradiol-binding proteins in both the MPOA-AH and MH. This change in ERalpha, ERbeta, and SHBG expression did not occur in the hippocampus. Both Northern blot and DNA sequence analysis confirmed the results of the RT-PCR for SHBG. SELDI-TOF MS analysis demonstrated that in vivo estradiol treatments resulted in dramatically decreased levels of SHBG in the hypothalamus and that a reduction in SHBG mRNA by estradiol treatment also resulted in a reduction in SHBG protein levels. Estradiol treatment also eliminated detectable SHBG from the neurohypophysis, suggesting that estradiol controls SHBG levels in this release site. That in vivo estradiol treatments had the same inhibitory effects on mRNA levels for SHBG and both ERs suggests similar translational control mechanisms for all three steroid-binding proteins in the brain. That estradiol treatments also reduced pituitary SHBG suggests that such treatment releases SHBG from the neurohypophysis.

Animals↗

Neonatal treatment with tamoxifen causes immediate alterations of the sexually dimorphic nucleus of the preoptic area and medial preoptic area in male rats.

Tamoxifen is an antiestrogen widely used for the treatment of breast cancer. Current evolutions in preventive strategies to include healthy premenopausal women warrant the study of its developmental toxicity. Perinatal treatment of male rodents with tamoxifen caused reproductive tract lesions and sexual behavior deficits similar to those induced by diethylstilbestrol (DES). Those abnormalities could originate, at least in part, from lesions of the hypothalamic-pituitary axis. The initial alterations caused by tamoxifen in the hypothalamic medial preoptic area (MPOA) and sexually dimorphic nucleus of the preoptic area (SDN-POA) were studied in 6-day-old male rat pups treated with 100 micrograms tamoxifen (group 1), 1 microgram DES (group 2) or vehicle (group 3) from PN1 to 5. In situ hybridization was performed to analyze the expression of the GAP-43 gene, a marker of neuronal differentiation, and morphometry was used to study the neuronal density in the SDN-POA and MPOA and the volume and number of neurons in the SDN-POA. Tamoxifen reduced severely the volume and neuron numbers in the SDN-POA (46.1% and 47.8% of controls, respectively). The neuronal density of the MPOA was not modified. GAP-43 gene expression was decreased as demonstrated by a greater percentage of unlabeled neurons (grade 0) mirrored by a lesser percentage of intensely labeled ones (grade 2) in the SDN-POA and MPOA. In contrast to the effects of the antiestrogen, DES did not affect the above endpoints. These data indicated that developmental exposure of male rat pups to tamoxifen-induced immediate neuronal loss in one and altered differentiation in two hypothalamic areas crucial to reproduction. How those initial alterations contribute to the pathogenesis of the reproductive disorders observed in the adult male needs further investigation.

Animals↗

Locus coeruleus lesions decrease norepinephrine input into the medial preoptic area and medial basal hypothalamus and block the LH, FSH and prolactin preovulatory surge.

The aim of this work was to study the role of the dorsal noradrenergic ascending pathway (DNAP), which originates in the locus coeruleus (LC) on the preovulatory surge of luteinizing hormone (LH) follicle-stimulating hormone (FSH) and prolactin (PRL) by producing bilateral electrolytic lesions (cathodal or anodal) in this nucleus. LC lesions were placed at 11.00 h on proestrus in female rats with regular 4-day estrous cycles. Intact rats, sham-operated as well as animals with missed lesions served as controls. In Experiment I, anodal current was applied and hourly blood samples were withdrawn (from 13.00 to 17.00 h) via a jugular catheter from conscious, freely moving rats for determination of plasma LH, FSH and PRL concentrations. In Expt. II, Expt. I was repeated using cathodal current and collecting blood samples hourly from 13.00 to 18.00 h. In both experiments the animals were sacrificed on the next morning when the occurrence of ovulation was checked. The medial septal area (MSA), medial preoptic area (MPOA), and medial basal hypothalamus (MBH) were dissected and assayed for norepinephrine (NE), dopamine (DA) and 5-hydroxyindoleacetic acid (5-HIAA) content. Experiment III was performed in order to test if a hormonal discharge occurred immediately after lesion placement. Blood samples were collected immediately before and 15, 30, 60 and 90 min postoperatively (from 11.00 to 12.30 h). Either anodal or cathodal lesions blocked the proestrous surge of LH, FSH and PRL. The hypothesis that the lesions advanced or delayed these hormonal surges was rejected since we found no increases in the hormonal levels from 11.00 to 12.30 or from 13.00 to 18.00 h, and ovulation was not observed on the following morning in the lesioned animals. Since control, sham-operated and missed-lesion groups exhibited LH, FSH and PRL surges and ovulation, this blockage appears to be caused by the destruction of the LC neurons. Also, this blockade was correlated with a decrease in the NA content in the MPOA and MBH, but not in the MSA, whereas the DA and 5-HIAA content were not changed in all groups examined. The results lead us to suggest that the integrity of noradrenergic afferent input from the LC to luteinizing hormone-releasing hormone neurons in the MPOA and MBH is essential for triggering the preovulatory surge mechanisms for gonadotrophins and PRL.

Animals↗

Evidence for vesicular glutamate transporter synapses onto gonadotropin-releasing hormone and other neurons in the rat medial preoptic area.

The medial preoptic area is a key structure in the control of reproduction. Several data suggest that excitatory amino acids are involved in the regulation of this function and the major site of this action is the medial preoptic region. Data concerning the neuromorphology of the glutamatergic innervation of the medial preoptic area are fragmentary. The present investigations were focused on: (i) the morphology of the vesicular glutamate transporter 1 (VGluT1)- and vesicular glutamate transporter 2 (VGluT2)-immunoreactive nerve terminals, which are considered to be specific to presumed glutamatergic neuronal elements, in the medial preoptic area of rat; and (ii) the relationship between these glutamate transporter-positive endings and the gonadotropin-releasing hormone (GnRH) neurons in the region. Single- and double-label immunocytochemistry was used at the light and electron microscopic level. There was a weak to moderate density of VGluT1- and a moderate to intense density of VGluT2-immunoreactive elements in the medial preoptic area. Electron microscopy revealed that both VGluT1- and VGluT2-immunoreactive boutons made asymmetric type synaptic contacts with unlabelled neurons. VGluT2-labelled, but not VGluT1-labelled, axon terminals established asymmetric synaptic contacts on GnRH-immunostained neurons, mainly on their dendrites. The present findings are the first electron microscopic examinations on the glutamatergic innervation of the rat medial preoptic area. They provide direct neuromorphological evidence for the existence of direct glutamatergic innervation of GnRH and other neurons in the rat medial preoptic area.

Animals↗

Identification of a sexually dimorphic neural population immunoreactive for calcitonin gene-related peptide (CGRP) in the rat medial preoptic area.

The medial preoptic area (MPOA) of the rat exhibits morphological sex differences and is implicated in sex-specific functioning and behaviour. Using immunocytochemistry, the distribution and numbers of cells containing calcitonin gene-related peptide (CGRP) were examined in the MPOA of adult male and female rats. In the intact female rat, CGRP-immunoreactive (-IR) cells were found in a continuum within the MPOA extending from the caudal aspects of the organum vasculosum of the lamina terminalis through the anteroventral periventricular nucleus (AVPv) to the region of the medial preoptic nucleus (MPN). An additional small group of CGRP-IR cells was noted at the level of the caudal MPNin the ventrolateral (VL) region. Compared with males, the AVPv and MPN regions of the female contained over 25-fold more CGRP-IR cells (P < 0.01). The VL region contained similar numbers of CGRP-IR cells in both sexes. Ovariectomy 1 month earlier, with or without subsequent 17-beta estradiol treatment, had no effect on the numbers or distribution of CGRP-IR cells in the MPOA. Gonadectomy of male rats resulted in a significant increase (P < 0.01) in the numbers of CGRP-IR cells in the AVPv and MPN regions. Subsequent administration of testosterone propionate for 1 week reduced (P < 0.05) numbers of CGRP-IR cells to levels observed in the intact male. Neurones containing CGRP in the VL group were not altered by gonadal steroid manipulation. This study shows that CGRP neurones in the AVPv/MPN region are sexually dimorphic.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Estrogen receptor beta modulates estradiol induction of progestin receptor immunoreactivity in male, but not in female, mouse medial preoptic area.

The medial preoptic area (mPOA) of the hypothalamus contains many neurons that express estrogen receptor alpha (ER) and/or ERbeta. We examined the distribution of these receptors and assessed responses to estradiol (E2) in the adult mouse mPOA. Gonadectomized adult male and female mice were killed, and brains were processed for immunocytochemistry for ERalpha and ERbeta. More ERalpha immunoreactive (-ir) than ERbeta-ir neurons were present in the mouse mPOA. Numbers of ERalpha-ir cells were equivalent between males and females, but males had significantly more ERbeta-ir neurons than females. Using breeders that were heterozygous for disrupted ERalpha and ERbeta genes, we produced offspring with varying numbers (0, 1, or 2) of functional and disrupted ERalpha and ERbeta genes. After gonadectomy, half the mice received E2 for 5 d before they were killed. Estradiol treatment, sex, and genotype each had independent effects on numbers of PR-ir neurons in the mPOA. In all cases, brains that lacked at least one functional copy of ERalpha had reduced PR-ir cell numbers. In gonadectomized, untreated mice, one functional copy of the ERbeta gene was correlated with the largest amount of PR-ir. After E2 treatment, both sexes had greatly enhanced numbers of PR-ir containing neurons. In females, maximal PR induction required the presence of at least one functional copy of ERalpha, whereas in males, at least a single copy of both functional ERbeta and ERalpha genes was needed for maximal PR-ir induction. We hypothesize that the two ERs have dependent and independent roles in sexual differentiation of neuroendocrine function.

Animals↗

The long lasting effects of electrical simulation of the medial preoptic area and medial amygdala on maternal behavior in female rats.

A program of repeated electrical (kindling-like) stimulation of the medial preoptic area (MPOA) or the medial amygdala (MedAmyg) on maternal and other behaviors were investigated. Stimulation was applied daily for 14 days (or until a stage 3 motor seizure was observed) using 2 s trains of biphasic square wave pulses at 60 Hz, 1 ms duration and 300-500 microA. Confirmation of afterdischarge using these parametres was established. In the first experiment, maternally experienced (but not post-partum) MedAmyg stimulated animals became maternal more slowly than did MedAmyg not stimulated animals or than MPOA stimulated animals. In the second experiment, virgin animals were used. MPOA stimulation enhanced the female's preference for pup associated environments in the conditioned place preference (CPP) paradigm. MedAmyg stimulation had no effect on CPP performance, but produced a decreased preference for pup odors in a modified hole board test and increased 'anxiety' in the open field. These results confirm that the MPOA and the MedAmyg are involved in facilitating and attenuating maternal responsiveness and related (precursor?) behaviors, respectively. It appears that chronic (kindling-like) stimulation of these neural substrates enhances their functions.

Amygdala↗

Intracranial androgenic activation of male-typical behaviours in house mice: concurrent stimulation of the medial preoptic area and medial nucleus of the amygdala.

This experiment examined whether testosterone proprionate (T) action in the medial preoptic area (MPO) would synergize with T action in the medial nucleus of the amygdala (AME) for the expression of androgen-dependent behaviors in house mice. Cannulae containing T were bilaterally implanted into the MPO, the AME, or both areas concurrently (MPO/AME) of castrated males. In addition, other castrates were implanted subcutaneously with empty Silastic capsules (BSIL) or Silastic capsules containing T (TSIL). All subjects were examined for the following androgen-dependent, male-typical behaviors: mounting, urinary scent marking, preference for female urine over male urine, preference for female over male conspecifics and ultrasonic mating vocalizations. MPO implants restored ultrasonic vocalizations and preference for females, but had little or no effect upon urine marking, mounting or preference for female urine. In contrast, AME implants were ineffective at restoring any of these male-typical behaviors. The combined MPO/AME implants were not more effective in restoring male-typical behaviors than MPO implants alone, thus providing no evidence for synergy in hormone action between these two brain areas. In general, castration (BSIL) resulted in low levels of all behaviors whereas systemic T replacement (TSIL) resulted in high levels of behavior, verifying the androgen-dependence of these behaviors. Group differences in male-typical behavior could not be accounted for by differences in general activity levels. Moreover, none of the brain-implanted groups had larger seminal vesicles than those of the BSIL. Thus, when the brain implants affected behavior, they most probably did so through their effects within the brain. Although the AME is a target for steroid hormones and is an important area for the expression of male-typical behaviors, intracranial T implants into the AME did not demonstrate a role for androgen in the AME in restoring male-typical behaviors in castrated mice.

Amygdala↗

Concurrent androgenic stimulation of the ventral tegmental area and medial preoptic area: synergistic effects on male-typical reproductive behaviors in house mice.

Cannulae containing testosterone proprionate (T) were bilaterally implanted into the medial preoptic area (MPO), the ventral tegmental area (VTA), or both areas concurrently (MPO/VTA) of castrated male house mice. A fourth group of castrates in which the intracranial implants missed their targets (MIMP) served as controls. In addition, other castrates were implanted subcutaneously with empty silastic capsules (BSIL) or silastic capsules containing T (TSIL). All subjects were examined for the following male-typical behaviors: mounting, attraction to female urine, ultrasonic mating vocalizations and urinary scent marking. In addition, the males were tested for activity levels to insure that they were not motorically impaired. In general, TSIL implants restored all male-typical behaviors to normal levels, whereas BSIL and MIMP implants were generally ineffective. Similar to previous findings, MPO implants alone completely restored ultrasonic vocalizations, partially restored urine marking, and had little or no effect upon mounting or urine preference. In contrast, VTA implants alone were ineffective at restoring any of these male-typical behaviors. However, the combined MPO/VTA implants were the most effective in restoring male-typical behaviors. In fact, a synergism between concurrent hormone action in the MPO and VTA was seen for mounting and urine preference. We interpret these data to indicate that androgen may act simultaneously in the MPO and VTA for more complete expression of some male-typical reproductive behaviors.

Animals↗

Conjugated estradiol increases female sexual receptivity in response to oxytocin infused into the medial preoptic area and medial basal hypothalamus.

The ovarian steroid estradiol (E) has been found to increase both receptor affinity and release of the neuropeptide oxytocin (OT) in plasma membrane preparations. Therefore, we hypothesized that E conjugated to bovine serum albumin at position 6 (E-6-BSA) would increase behavioral responsiveness to OT. Preliminary results showed that 200 ng/microl of E-6-BSA increased sexual receptivity slightly, but not significantly. Therefore, this dose was used as a subthreshold dose to test whether it would increase sexual responsiveness when infused in combination with 100 ng/microl OT. After recovery from cannula implantation surgery animals were injected with 0.5 microg E benzoate daily for 3 days before testing. On the fourth day, after a baseline preinfusion test rats were infused bilaterally with E-6-BSA alone or with OT, OT with BSA, or conjugated progesterone, luteinizing hormone-releasing hormone equimolar to OT alone, or with E-6-BSA or conjugated progesterone alone. When infused into either the medial preoptic area-anterior hypothalamus or the medial basal hypothalamus the combination of OT and E-6-BSA significantly increased sexual receptivity over receptivity after artificial cerebrospinal fluid control infusions. Neither bilateral infusions of OT in combination with conjugated progesterone nor E-6-BSA in combination with luteinizing hormone-releasing hormone enhanced sexual receptivity. Results presented here strongly support the conclusion that some of the effects that E has in sensitizing brain systems to the facilitating effects of OT occur at the membrane level in the medial preoptic area-anterior hypothalamus and medial basal hypothalamus.

Animals↗

Effects of clonidine and phentolamine infused into the medial preoptic area and medial basal hypothalamus of the guinea pig.

In ovariectomized (OVX) female guinea pigs sequential administration of estradiol and then progesterone (P) is usually necessary to induce the sexually receptive lordosis posture. Systemic administration of alpha-adrenergic agonists can induce lordosis in OVX guinea pigs primed with estradiol benzoate (EB) alone and facilitate lordosis in OVX females primed with EB and P. In this study, we examined the regional specificity of this regulation by infusing the alpha-adrenergic agonist clonidine (CLON) or the alpha-adrenergic antagonist phentolamine (PHEN) into discrete brain areas. CLON, infused in the medial basal hypothalamus (MBH) of EB-primed females, increased the percentage of females showing lordosis 15-45 min after infusion (p < 0.05) and also increased the number of seconds females held the lordosis posture 15 min to approximately 2.0 h after infusion (by as much as 65% at 15 min p < 0.001). CLON infused in the medial preoptic area (MPOA) of EB primed females had no effect on lordosis except at 4.0 h after infusion when it increased the number of seconds females held the lordosis posture (p < 0.05). In EB + P primed females, PHEN infused into the MBH transiently reduced the number of seconds EB + P primed females held lordosis from 30 min to approximately 2.0 h after infusion (by as much as 64% at 1.0 h; p < 0.01). Conversely, PHEN infused into the MPOA of EB + P primed females transiently increased the number of seconds females held lordosis from 15 min to 2.0 h after infusion (maximum difference 64%; p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

Effects of alpha-2-adrenergic drugs in the medial preoptic area and medial basal hypothalamus on lordosis in the guinea pig.

We have recently demonstrated that (1) stimulation of alpha-adrenergic neurotransmission in the medial basal hypothalamus (MBH) of ovariectomized (OVX) estradiol-17 beta-benzoate (EB) treated female guinea pigs activates lordotic responding and that (2) inhibition of alpha-adrenergic neurotransmission in the MBH inhibits lordotic responding in EB and progesterone (EB + P) treated females (Neuroendocrinology, in press). In this study, we investigated the relative influence of selective drugs altering alpha-2-adrenergic neuronal transmission within the MBH and medial preoptic area (MPOA) on lordotic responding in EB + P primed females. In EB + P primed females the selective alpha-2-adrenergic agonist UK-14,304 increased the number of seconds EB + P treated females held lordosis at test periods starting 15 min after infusion until test periods 1.5 h after infusion into the MPOA (maximum effect at test period 30 min after infusion, 265% vehicle (VEH); P < 0.005). UK-14,304 also facilitated lordotic responding 15-30 min and 1.5 h after infusion into the MBH of EB + P primed females (maximum effect at test period 30 min after infusion, 223% VEH; P < 0.025). Furthermore, infusing the selective alpha-2-adrenergic antagonist yohimbine (YOH) into the MBH of EB + P primed females inhibited lordotic responding between 1.0 and 2.0 h after treatment (maximum 1.5 h, 42% VEH; P < 0.05). These results demonstrate that alpha-2-adrenergic neurotransmission within the regions of the MPOA and the MBH facilitates lordotic responding in the guinea pig.

Adrenergic alpha-Agonists↗

Testosterone stimulation of the medial preoptic area and medial amygdala in the control of male hamster sexual behavior: redundancy without amplification.

Receptors for gonadal steroids are present in an interconnected network of limbic nuclei. The existence of this network structure has important implications for how steroids control reproductive physiology and behavior. In 1986, Cottingham and Pfaff proposed that properties of a steroid-responsive neural network could include redundancy, amplification, stability and selective filtering. The present study tested the concept of steroid amplification, using male hamster sexual behavior as a model. In the male hamster, the medial amygdaloid nucleus (Me) and medial preoptic area (MPOA) are essential for mating behavior, and both nuclei transduce steroid cues to facilitate copulation. To determine if steroid action at multiple interconnected nuclei amplifies mating, the present study compared sexual behavior in castrated male hamsters bearing unilateral intracranial implants of testosterone in Me or MPOA with that of males with dual testosterone implants in Me and MPOA. Implants that stimulated androgen receptor-containing neurons in Me or MPOA stimulated copulatory behavior above castrate levels. However, behavior of males with dual implants was not significantly different from that of males with single implants. This suggests that steroid action at either MPOA or Me is sufficient to facilitate mating, but dual stimulation of these reciprocally-connected nuclei does not amplify sexual behavior.

Amygdala↗

Some characteristics of the darkly stained area of the medial preoptic area of rats.

Male rats have larger darkly stained area (DSA) within the medial preoptic area (MPOA) than female rats and this sex difference appears at the age of day 5 and continues to persist up to senescence. This sex dimorphism seems to be independent of gonadal hormones in the adult. In male rats the DSA has higher neuron density and larger neurons than the surrounding non-DSA. The total neuron number in MPOA is not different between young male rats and young female rats. In old age, neuron number of MPOA decreased in female rats but not in male rats.

Aging↗

Gating of the dorsal penile nerve inputs by norepinephrine at the medial preoptic area in rats.

The medial preoptic area neurons related to male sexual behaviour in rats were identified by their responses to dorsal penile nerve stimulation. These neurons were further tested with norepinephrine applied iontophoretically. From the 21 medial preoptic area neurons recorded in urethane anaesthetized rats, 17 neurons responded to dorsal penile nerve stimulation. Excitatory and inhibitory responses were found in almost equal number of neurons. 14 neurons responded to norepinephrine application, out of which six neurons were excited and eight were inhibited. The direction of changes produced by dorsal penile nerve stimulation and norepinephrine application were similar in 10 neurons. The results suggest that the sensory inputs from the genitalia are possibly gated by norepinephrine at the level of the medial preoptic area. Afferent information from the genitalia carried by dorsal penile nerve and the availability of norepinephrine at the level of the medial preoptic area probably help in maintaining adequate level of sexual arousal.

Action Potentials↗

Branching projections from subcoeruleus area neurons to medial preoptic area and cervical spinal cord revealed by double retrograde neuronal labeling.

In this study we utilized a double retrograde axonal tracing technique to investigate the possible existence of collateralized axonal projections of subcoeruleus area neurons to both 'medial preoptic area (MPA) and cervical (C1-C3) spinal cord'. Following microinjections of fluorescent tracers (Fast blue (FB) and Diamidino yellow (DY) within MPA and C1-C3, substantial numbers of FB and DY single-labeled neurons as well as FB-DY double-labeled branched neurons have been found within subcoeruleus area.

Amidines↗

[Ultrastructural organization of the hypothalamic medial preoptic area and its changes under the effect of pyrogens].

In order to study structural bases of central mechanisms of thermoregulation, a comparative electron microscopic analysis of various cellular groups in one of thermosensitive zones of the cat hypothalamic area--the medial preoptic area--have been carried out under conditions of experimental fever. The latter is produced by injection of pyrogen of bacterial origin--pyrogenal--to the animals. Pyrogenal, increasing the body temperature, produces a stimulatory effect on various cellular elements, first of all on leucocytes, monocytes and macrophages in the medial preoptic area, as well as on endotheliocytes of the terminal vessels. Under pyrogenal effect activation of microglial cells and pericytes also takes place, and as a result of the rearrangements, occurring in the structure, they change into macrophages. This is an evidence of their active participation in the immune protection of the brain. According to the data from other investigations, all these activated cells produce peptide interleukin-1, one of the mediators of fever and stimulator of the immune system. Pyrogenal is stated to produce a stimulating effect on the astroglia and on some neurons of the medial preoptic area, that respond with cytoplasm increase and accumulation of numerous organelles. The reactive changes at fever in some neurons of the medial preoptic area can demonstrate that they belong to the thermosensitive pool. A conclusion is made, concerning a complex effect of pyrogenal, that results in a cooperative response of a number of cellular systems of the organism.

Animals↗

Estrogen receptor alpha expression in the medial preoptic area and the medial basal hypothalamus under different physiological conditions in cattle.

The distribution and morphology of immunoreactive estrogen receptor alpha (ERalpha)- containing cells were examined in the cattle brain. The brains were collected from two cows and a male calf. One of the cows was sacrificed one week after parturition. ERalpha expressions in the preoptic area of the rostral forebrain and the medial basal hypothalamic area were evaluated immunohistochemically using a mouse monoclonal antibody. In all animals, the signals that indicate ERalpha were detected in the medial preoptic area, the level of the organum vasculosum of the lamina terminalis and the bed nucleus of the stria terminalis. In the caudal hypothalamic region, they were detected in the arcuate nucleus, the periventricular and ventromedial hypothalamic nuclei. ERalpha-containing cells were characterized by a dense nuclear reaction product. In all the subjects examined, ERalpha signals were clearly detected in the cytoplasm as well. The density of ERalpha expression was different among the three cattle; the number of ERalpha containing cells in the postpartum cow was much lower than that in the other cow and the male calf. The present findings suggest that ERalpha expression in the forebrain is influenced by the reproductive status in the cattle.

Animals↗