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Colocalization of estrogen receptor alpha and NMDA-2D mRNAs in amygdaloid and hypothalamic nuclei of the mouse brain.

Interactions between gonadal steroid hormones and glutamatergic neurons participate in limbic and hypothalamic functions. Glutamate receptors are divided into metabotropic and ionotropic receptors. Among ionotropic receptors, N-methyl-D-aspartate (NMDA) is involved in a variety of neurophysiological processes. In turn, NMDA receptors are composed of subunits from two families: NR1 and NR2. Recently, molecular studies have shown that the expression of NMDA-2D receptor is regulated by estrogen. Although the expression patterns of NMDA-2D and ERalpha in the rodent brain appear to overlap, it remained to be determined whether or not these two receptors co-exist, in vivo, at the level of single neurons. To test the hypothesis that NMDA-2D and ERalpha messenger ribonucleic acid (mRNA) are co-expressed in the same neurons of the adult mouse brain, we used a dual-label in situ hybridization technique. Neuronal populations were identified with digoxigenin-tagged complementary RNA probes for NMDA-2D and 35S-labeled cRNA probes for ERalpha. Our results demonstrate that a majority of the ERalpha-positive neurons also express NMDA-2D mRNA. Quantitative examination of the cellular expression in the ventromedial and arcuate nuclei of the hypothalamus (VMH and Arc) showed that 52.5% and 61.5%, respectively, of the neurons endowed with ERalpha mRNA also contain NMDA-2D mRNA. In the amygdala, 51% of ERalpha-positive cells also contain NMDA-2D mRNA. These findings provide the first anatomical evidence that ER and NMDA-2D receptors can be found in the same hypothalamic and amygdaloid neurons. Co-expression of ERalpha and NMDA-2D receptors supports the hypothesis of the interactions between glutamate receptors and estrogens in brain regions where estrogens control female reproductive behaviors and neuroendocrine functions.

Amygdala↗

Gene transfer and in vivo promoter analysis of the rat progesterone receptor using a herpes simplex virus viral vector.

The progesterone receptor (PR) gene is expressed in cells of the anterior pituitary and hypothalamus, and PR levels are regulated by estrogen (E) in a tissue-specific fashion. To demonstrate that E induces transcription via the PR promoter, and to identify sequences within the PR promoter responsible for tissue-specific and hormonal regulation, we have utilized a defective herpes simplex virus vector for direct gene transfer into the rat pituitary and brain. We designed a viral amplicon expressing the beta-galactosidase gene under the regulation of a 2.1-kb PR promoter fragment to create a defective viral vector for gene transfer into the brain. Following injection of this vector into the pituitary and brain, its pattern of expression and ability to respond to estradiol 3-benzoate (EB) were examined. In the pituitary, lacZ activity was observed in cells of the anterior lobe (AL). However, no activity was seen in the neurointermediate lobe (NIL), demonstrating tissue specific transcriptional regulation. A approximately sixfold increase in cells demonstrating beta-galactosidase activity was observed in the AL following treatment with EB. Likewise, injection of defective viral vector into the hypothalamus followed by treatment with EB resulted in a approximately eightfold increase in cells demonstrating beta-galactosidase activity including the very cell groups responsible for EB-dependent reproductive behavior. In contrast, no vector dependent activity was observed in the caudate nucleus, a tissue with no endogenous expression of PR, despite polymerase chain reaction evidence demonstrating the presence of the vector in this tissue. These results demonstrate that the 2.1-kb PR promoter fragment contains the sequence information required for correct tissue and hormonal regulation of PR.

Animals↗

Estrogen receptor alpha forms estrogen-dependent multimolecular complexes with insulin-like growth factor receptor and phosphatidylinositol 3-kinase in the adult rat brain.

Estradiol and insulin-like growth factor-I (IGF-I) have numerous functional interactions in the brain, including the regulation of neuroendocrine events, the control of reproductive behavior and the promotion of synaptic plasticity and neuronal survival. To explore the mechanisms involved in these interdependent actions of estradiol and IGF-I in the adult brain, the potential interactions of estrogen receptors with components of the IGF-I signaling system were assessed in this study. Systemic estradiol administration resulted in a transient immunocoprecipitation of the IGF-I receptor with the estrogen receptor alpha and in a transient increase in tyrosine phosphorylation of the IGF-I receptor in the hypothalamus of adult ovariectomized Wistar rats. Both effects were coincident in time, with a peak between 1 and 3 h after systemic estradiol administration. Three hours after estradiol treatment, there was an enhanced immunocoprecipitation of estrogen receptor alpha with p85 subunit of phosphatidylinositol 3-kinase, as well as an enhanced immunocoprecipitation of p85 with insulin receptor substrate-1. The interaction with the IGF-I receptor was specific for the alpha form of the estrogen receptor and was also induced by intracerebroventricular injection of IGF-I. These hormonal actions may be part of the mechanism by which estradiol activates IGF-I receptor signaling pathways in the brain and may explain the interdependence of estrogen receptors and the IGF-I receptor in synaptic plasticity, neuroprotection and other neural events.

Animals↗

Estrogen regulation of mu-opioid receptor mRNA in the forebrain of female rats.

Previous studies have suggested that opioids play a role in the regulation of reproductive behaviors in the female rat. The present study examined whether estrogen treatment alters mu-opioid receptor mRNA levels in different areas of the forebrain of ovariectomized (OVX) female rats using the in situ hybridization technique. We observed an increase in mu-opioid receptor mRNA levels in the ventromedial nucleus of the hypothalamus (VMH) and arcuate nucleus (ARN) after 48 h of 10 microg of 17-beta-estradiol-3-benzoate treatment when compared to OVX females. No effects of estrogen were observed on mu-opioid receptor mRNA levels in the posterior medial nucleus of the amygdala (MeAmyg), hippocampus, caudate-putamen (CPu) or the medial habenula. Our result suggests that the estrogenic regulation of mu-opioid receptor in the CNS may in part be mediated by de novo synthesis and/or stability of the mu-opioid receptor message.

Animals↗

Molecular cloning of a cDNA encoding a potential water-borne pheromonal attractant released during Aplysia egg laying.

Recently deposited egg cordons are a source of water-borne pheromones that attract the marine mollusk Aplysia into breeding aggregations and coordinate male and female reproductive behavior within the aggregation. A potential pheromonal attractant has been isolated from egg cordon eluates and the peptide partially characterized [S.D. Painter, B. Clough, X. Fan, G.T. Nagle, Soc. Neurosci. Abstr., Vol. 22 (1996) 837]. Using this information, we have cloned an Aplysia albumen gland cDNA that encodes a precursor protein containing a single copy of the full-length peptide, and demonstrated that there are abundant levels of pheromone mRNA transcripts (0.8 and 2.5 kb) in the albumen gland. This is consistent with the reported function of the gland (i.e. packaging the eggs into a cordon for deposition), with behavioral studies showing that the albumen gland is a potential source of attractants, and more recent biochemical studies in which the full-length peptide has been isolated from the albumen gland. This is the first candidate peptide pheromone in mollusks and the first in invertebrates. The pheromonal regulatory system in Aplysia may provide a model system for examining the structural characteristics of peptide pheromones.

Amino Acid Sequence↗

GABA augments basal and electrically stimulated 3H-norepinephrine release in hypothalamic, preoptic area and cortical slices of female rats.

These studies examined the regulation by GABA of norepinephrine release from hypothalamus, preoptic area and frontal cortex. Using superfused brain slices from female rats, we show that 100 microM GABA enhances both basal and electrically stimulated release of 3H-norepinephrine in all three brain regions. The GABAA agonist muscimol (100 microM) significantly augments 3H-norepinephrine release, but it is somewhat less effective than GABA. The GABAB agonist baclofen has little or no effect on basal 3H-norepinephrine efflux. GABA also augments both the magnitude and duration of electrically evoked 3H-norepinephrine release in slices from all three brain regions. GABA facilitation of electrically stimulated 3H-norepinephrine release is mediated through GABAA receptors as evidenced by its blockade by 10 microM bicuculline, a GABAA antagonist, but not by 200 microM 2-OH-saclofen, a GABAB antagonist. These data show that the inhibitory amino acid neurotransmitter GABA enhances both basal and evoked release of 3H-norepinephrine in brain slices from female rats. These effects are predominantly mediated by GABAA receptors. GABA modulation of hypothalamic norepinephrine release may play a role in the regulation of gonadotropin secretion and reproductive behaviors such as lordosis.

Animals↗

Localization of alpha1B-adrenergic receptor in female rat brain regions involved in stress and neuroendocrine function.

Activation of alpha1-adrenergic receptors has been linked to the control of blood pressure, neuroendocrine secretion, reproductive behavior and mood. The present study describes the distribution of alpha1B-adrenergic receptor immunoreactivity in female rat brain regions involved in stress and neuroendocrine function. The pattern of immunolabeling seen resembles that obtained in previous in situ hybridization studies. Several hypothalamic areas that control pituitary function showed intense fiber and/or cell immunolabeling, including the paraventricular nucleus of the hypothalamus, the supraoptic nucleus, and the median eminence. Some regions such as the arcuate nucleus, the median eminence, and dorsal hypothalamus exhibit intense labeling of axonal varicosities, while other regions exhibit only perikarya immunolabeling. alpha1B-adrenergic receptor immunoreactivity was also observed in large pyramidal neurons of layer V of the cerebral cortex, the frontal cortex showing a particularly strong immunoreactivity. Virtually all thalamic regions were labeled, especially the lateral and ventral areas. In addition, labeled cells were present in hippocampus, the medial septum, the horizontal and vertical limbs of the diagonal band of Broca, and the caudate putamen. Finally, some midbrain and hindbrain regions important for motor function were immunoreactive. Because ligands specific for alpha1-adrenergic receptor subtypes are not available, the present immunocytochemical study not only addresses the subcellular and regional distribution of alpha1B-adrenergic receptors but may also provide clues about receptor subtype-specific function.

Animals↗

What explains rural-urban differentials in child mortality in Brazil?

This paper presents an analysis of differentials in child survival by rural-urban place of residence in Brazil and examines the hypothesis that observed mortality differentials by place of residence are merely manifestations of underlying differences in socioeconomic status and demographic and reproductive behavior. The child mortality data come from the 1986 Demographic and Health Survey of Brazil and supplementary community-level variables are obtained from a database assembled by the Brazilian federal statistical agency. Child mortality rates are substantially and significantly lower in urban areas of Brazil. Our results suggest, however, that the urban advantage does not simply reflect underlying differences in socioeconomic and behavioral characteristics at the individual and household levels; rather, community variables appear to play an independent and important role. We also find that the effects of community characteristics on child survival are moderated by household socioeconomic factors, especially maternal education. Differences in socioeconomic characteristics are therefore important in explaining rural-urban child mortality differentials, but not in the way hypothesized by previous researchers.

Adolescent↗

Neuroprotection by estradiol.

This review highlights recent evidence from clinical and basic science studies supporting a role for estrogen in neuroprotection. Accumulated clinical evidence suggests that estrogen exposure decreases the risk and delays the onset and progression of Alzheimer's disease and schizophrenia, and may also enhance recovery from traumatic neurological injury such as stroke. Recent basic science studies show that not only does exogenous estradiol decrease the response to various forms of insult, but the brain itself upregulates both estrogen synthesis and estrogen receptor expression at sites of injury. Thus, our view of the role of estrogen in neural function must be broadened to include not only its function in neuroendocrine regulation and reproductive behaviors, but also to include a direct protective role in response to degenerative disease or injury. Estrogen may play this protective role through several routes. Key among these are estrogen dependent alterations in cell survival, axonal sprouting, regenerative responses, enhanced synaptic transmission and enhanced neurogenesis. Some of the mechanisms underlying these effects are independent of the classically defined nuclear estrogen receptors and involve unidentified membrane receptors, direct modulation of neurotransmitter receptor function, or the known anti-oxidant activities of estrogen. Other neuroprotective effects of estrogen do depend on the classical nuclear estrogen receptor, through which estrogen alters expression of estrogen responsive genes that play a role in apoptosis, axonal regeneration, or general trophic support. Yet another possibility is that estrogen receptors in the membrane or cytoplasm alter phosphorylation cascades through direct interactions with protein kinases or that estrogen receptor signaling may converge with signaling by other trophic molecules to confer resistance to injury. Although there is clear evidence that estradiol exposure can be deleterious to some neuronal populations, the potential clinical benefits of estrogen treatment for enhancing cognitive function may outweigh the associated central and peripheral risks. Exciting and important avenues for future investigation into the protective effects of estrogen include the optimal ligand and doses that can be used clinically to confer benefit without undue risk, modulation of neurotrophin and neurotrophin receptor expression, interaction of estrogen with regulated cofactors and coactivators that couple estrogen receptors to basal transcriptional machinery, interactions of estrogen with other survival and regeneration promoting factors, potential estrogenic effects on neuronal replenishment, and modulation of phenotypic choices by neural stem cells.

Estradiol↗

Localization of molluscan cardioexcitatory tetrapeptide in the brain of African Cichlid fish (Haplochromis burtoni) revealed by immunocytochemistry.

The FMRFamide-like immunoreactivity was investigated in the brain of African cichlid fish, Haplochromis burtoni, in which sexual maturation is under social control. In both dominant and subdominant males and females, the FMRFamide immunoreactive (ir) cells were found only in the nucleus olfacto-retinalis and in the nucleus of the midbrain tegmentum. However, several FMRFamide-ir fibers were seen in the olfactory bulb and throughout the entire brain of both male morphs and female fish. As the role of nucleus olfacto-retinalis is well known in chemoreception, these results suggest the involvement of FMFRamide-like peptide in the chemosensory control of reproductive behavior in this species.

Animals↗

Estrogen receptor-immunoreactive neurons in the lumbosacral cord projecting to the periaqueductal gray in the ovariectomized female cat.

The periaqueductal gray (PAG) plays a crucial role in reproductive behavior. The present study investigates whether lumbosacral PAG-projecting neurons contain estrogen receptors. In four ovariectomized adult female cats, injections with cholera toxin subunit (CTb) were made into the PAG to retrogradely label PAG projecting neurons in the lumbosacral cord. Estrogen receptor immunoreactive ER-IR neurons in the lumbosacral cord were identified immunohistochemically using the antibody H222. PAG-projecting neurons that were immunoreactive for the estrogen receptor were very scarce, and predominantly present in the medial part of the ventral horn. The results indicate that only very few of the neurons relaying information from the urogenital organs to the PAG contain estrogen receptors.

Animals↗

Estrogen receptor-alpha-immunoreactive neurons in the periaqueductal gray of the adult ovariectomized female cat.

Anatomical and physiological studies in rodent and cat have shown that distinct parts of the midbrain periaqueductal gray (PAG) are important for the estrogen dependent, female reproductive behavior. The present study gives a detailed overview of the estrogen receptor-alpha-immunoreactive (ER-IR) neurons in the PAG in the cat. ER-IR neurons were found throughout the rostrocaudal extent of the PAG and laterally adjacent tegmentum, but were most numerous at caudal levels. The lateral and dorsal PAG contained most ER-IR neurons, whereas moderate numbers were found dorsolaterally. In these areas, only very few ER-IR neurons were found near the border of the ependymal layer. Except for the rostral dorsal raphe nucleus, the ventral PAG contained only few ER-IR neurons.

Animals↗

Diencephalic neurons producing melanin-concentrating hormone are influenced by local and multiple extra-hypothalamic tachykininergic projections through the neurokinin 3 receptor.

As melanin-concentrating hormone (MCH) neurons express the neurokinin 3 receptor (NK3) in the rat diencephalon, their innervation by tachykininergic fibers, the origin of this innervation and the effect of a NK3 agonist on MCH mRNA expression were researched. The obtained results show that the tachykininergic system develops complex relationships with MCH neurons. Overall, MCH cell bodies appeared targeted by both NKB- and SP-inputs. These afferents have multiple hypothalamic and extra-hypothalamic origins, but a local (intra-lateral hypothalamic area) origin from small interneurons was suspected as well. MCH cell bodies do not express NK1, but around 2.7% of the MCH neurons contained SP after colchicine injection. Senktide, a NK3 agonist, produced an increase of the MCH mRNA expression in cultured hypothalamic slices. This effect was reversed by two NK3 antagonists. Tachykinins enhance MCH mRNA expression, and, thus, may modulate the effect of MCH in functions such as feeding and reproductive behaviors in which this peptide has been experimentally involved.

Animals↗

Opiate receptors modulate estrogen-induced cholecystokinin and tachykinin but not enkephalin messenger RNA levels in the limbic system and hypothalamus.

Cholecystokinin, substance P and methionine enkephalin all regulate the display of reproductive behaviour. Their expression is exquisitely regulated by estrogen in the limbic-hypothalamic circuit, a circuit that regulates the display of estrogen-sensitive female reproductive behavior. Relatively little is known, however, about the interaction of endogenous opioid peptides with cholecystokinin and substance P in the limbic-hypothalamic circuit. Opiates antagonize the release of cholecystokinin and substance P in the hypothalamus and periaqueductal gray and stimulate cholecystokinin messenger RNA levels in the amygdala. To determine the effect of endogenous opioid input on estrogen-induced cholecystokinin, enkephalin and substance P expression, in situ hybridization histochemistry was used to examine estrogen-induced messenger RNA levels of these neuropeptides in specific nuclei of the limbic system and hypothalamus in the presence of opiate receptor antagonists. Estrogen treatment of ovariectomized rats significantly elevated cholecystokinin messenger RNA levels in the central portion of the medial preoptic nucleus, the encapsulated portion of the bed nucleus of the stria terminalis and the posterodorsal medial amygdala, as well as increased preproenkephalin and preprotachykinin messenger RNA levels in the ventromedial hypothalamic nucleus and the posterodorsal medial amygdala. The universal opiate receptor antagonist naltrexone and the delta-opiate receptor antagonist naltrindole each potentiated the estrogen-induced increase and elevated cholecystokinin messenger RNA levels an additional 1.9- to 2.8-fold depending on the nucleus examined, but had no effect on the estrogen-induced expression of either preproenkephalin or preprotachykinin messenger RNA. beta-Funaltrexamine, a mu-opiate receptor antagonist, had no effect on the medial preoptic or medial amygdaloid cholecystokinin messenger RNA levels or on the estrogen-induced expression of preproenkephalin messenger RNA but did cause a decrease in estrogen-induced cholecystokinin messenger RNA levels in the bed nucleus of the stria terminalis and a decrease in the preprotachykinin messenger RNA levels in the ventromedial hypothalamic nucleus. These results indicate that endogenous opioids, acting on the delta-opiate receptor within nuclei of the limbic-hypothalamic circuit, restrain the estrogen-induced increase of cholecystokinin messenger RNA expression. Activation of the mu-opiate receptor, however, may facilitate cholecystokinin messenger RNA expression in the bed nucleus of the stria terminalis and preprotachykinin messenger RNA expression in the ventromedial hypothalamic nucleus. Thus, endogenous opioid peptides may act in a site- and receptor-specific manner to modulate estrogen-induced neuropeptide levels in the limbic system and hypothalamus.

Animals↗

Glial fibrillary acidic protein immunodetection and immunoreactivity in the anterior and posterior medial amygdala of male and female rats.

The medial amygdala (MeA) has receptors for gonadal hormones and modulates reproductive behaviors in rats. Adult male and female rats were used for the immunodetection, a less accurate technique, and the immunohistochemistry for the astrocytic marker glial fibrillary acidic protein (GFAP) in the anterior and posterior MeA. Both procedures were done using polyclonal anti-GFAP and were quantified by densitometry. The first technique provided no evidence for a difference between sexes in the immunocontent of GFAP in any region of the MeA (p > 0.1). Nevertheless, the measure of the intensity of GFAP immunoreactivity (GFAP-IR) showed that females had a higher GFAP-IR in the posterodorsal (p < 0.01) and in the posteroventral subregions of the MeA (p < 0.01) than males. No sex difference was found in its anterodorsal part (p > 0.1). The present results point out the differences between these two above-mentioned techniques but add a new finding to the previously described sexual dimorphism in the MeA, i.e., the GFAP-IR. Data also suggest that probably astrocytes can be affected by sex steroids in this brain area. It is likely that this regionally specific difference in the GFAP-IR may contribute to the distinct functional roles that the MeA subregions have in male and female rats.

Amygdala↗

Regulation of aromatase gene expression in the adult rat brain.

Brain aromatase plays an important role in the regulation of adult reproductive behavior in male rodents. This report focuses on recent experiments from our laboratory that examined the distribution and regulation of aromatase mRNA in the rat brain. Aromatase mRNA was measured by a highly sensitive ribonuclease protection assay using a 32P-labeled antisense RNA probe that was complimentary to the 5' coding region of rat aromatase mRNA. This probe protects two RNA fragments in rat brain tissue: a 430-nt length fragment and a shorter 300-nt fragment. The presence of the 300-nt RNA fragment is not associated with enzyme activity in the rat brain and appears to represent an alternative brain-specific aromatase transcript whose function, if any, is unknown. In contrast, the 430-nt RNA fragment represents mRNA, which is thought to encode functional aromatase enzyme because its levels are correlated with aromatase activity concentrations in preoptic area, hypothalamus, amygdala, and ovary. Aromatase activity and mRNA levels in the preoptic area and hypothalamus decreased by 7 days after castration and were maintained at intact levels by treatment with testosterone and dihyhdrotestosterone, but not with estradiol. In contrast, neither aromatase activity nor mRNA levels in the amygdala are affected by castration or hormone replacement. In addition, sex differences in the regulation of aromatase mRNA were apparent in both the preoptic area and hypothalamus. These results demonstrate that androgens regulate the transcription or stability of aromatase mRNA in specific brain areas. Moreover, they suggest that gender differences in androgen responsiveness play an important role in regulating gene expression in the adult rat brain.

Alternative Splicing↗

The rally call recognition in males of two hybridizing partridge species, red-legged (Alectoris rufa) and rock (A. graeca) partridges.

The red-legged (Alectoris rufa) and rock (A. graeca) partridges hybridize and produce fertile offspring along a contact zone in French Southern Alps. The rally call emitted during pair formation, could play an important role in species recognition, acting as a behavioral reproductive isolating mechanism between males and females. In the present study, the coding system of the rally call was investigated from captive males of the two species and from F1 hybrids. By playing-back natural signals, we found that the two species as well as hybrid males responded to Alectoris signals but not to another species belonging to the Phasianidae family (Colinus virginianus). Results also indicate that red-legged and rock partridges responded stronger to conspecific calls than to heterospecific ones. However, they reacted similarly to conspecific and hybrid calls. F1 hybrids responded stronger to hybrids calls than to the two species ones. They did not distinguish the two parental species signals from each other. Although the two species showed the ability to discriminate the conspecific from the heterospecific signal, they clearly responded to the other species. This behaviour may play a role in the hybridization phenomenon.

Journal Article↗

Probabilistic hazard assessment of environmentally occurring pharmaceuticals toxicity to fish, daphnids and algae by ECOSAR screening.

The risks associated with occurrence of pharmaceuticals in water resources are mostly unknown. In the absence of extensive toxicological data, we scanned all the compounds observed in the environment for toxicological properties by (Quantitative) Structure Activity Relationship ((Q)SAR). The results of the probabilistic distribution of environmental and effect concentrations and hazard quotients (HQs) do not indicate significant acute risks prior to application of assessment factors. Compared with measured effect concentrations SAR predictions were more "sensitive" 80% of the time. The long-term effects of subtle and chronic changes, additive or synergistic effects and effects on other endpoints e.g. reproduction, behavior, metabolism, bacterial resistance etc. are still uncertain. (Q)SAR's can be important prioritization tools for subsequent experimental risk assessment of pharmaceuticals in surface waters, due to the prevalent lack of ecotoxicological data.

Animals↗