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      Effects of Estrogen in the Male Rat Medial Amygdala: Infusion of an Aromatase Inhibitor Lowers Mating and Bovine Serum Albumin-Conjugated Estradiol Implants Do Not Promote Mating

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          In male rats, copulatory behavior depends on estrogen-responsive neurons located in brain areas known to be crucial for mating. Blocking the aromatization of testosterone (T) to estradiol (E<sub>2</sub>) either throughout the brain or within the medial preoptic area (MPO) reduces mating, whereas E<sub>2</sub> treatment of either the MPO or the medial amygdala (MEA) maintains sexual behavior. The effects of T aromatization in the MEA have received less attention; therefore, 2 studies were done to further elucidate the effects of E<sub>2</sub> in the MEA. In experiment 1, gonadally intact male rats that showed robust mating behavior were administered chronic fadrozole, a nonsteroidal aromatase inhibitor, to the MEA to stop the conversion of T to E<sub>2</sub> and then paired with receptive females. Infusion of fadrozole to the MEA significantly lowered mating behavior in experimental males compared to vehicle-infused control males. To further investigate the mechanism by which E<sub>2</sub> acts in the MEA, in experiment 2, E<sub>2</sub> conjugated to bovine serum albumin (BSA-E<sub>2</sub>: a complex of E<sub>2 </sub>and a large protein that does not cross the plasma membrane, thereby restricting the action of E<sub>2</sub> to cell-surface signaling) was chronically administered bilaterally to the MEA of castrated, dihydrotestosterone-treated males. This treatment did not maintain mating behavior. These studies show that E<sub>2</sub> acts in the MEA to promote male sexual behavior and suggest an intercellular mechanism of E<sub>2</sub> action.

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          Most cited references 46

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          Cloning of a novel receptor expressed in rat prostate and ovary.

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            Mitochondrial localization of estrogen receptor beta.

             S-H. Yang,  R. Liu,  E Perez (2004)
            Estrogen receptors (ERs) are believed to be ligand-activated transcription factors belonging to the nuclear receptor superfamily, which on ligand binding translocate into the nucleus and activate gene transcription. To date, two ERs have been identified: ERalpha and ERbeta. ERalpha plays major role in the estrogen-mediated genomic actions in both reproductive and nonreproductive tissue, whereas the function of ERbeta is still unclear. In this study, we used immunocytochemistry, immunoblotting, and proteomics to demonstrate that ERbeta localizes to the mitochondria. In immunocytochemistry studies, ERbeta was detected with two ERbeta antibodies and found to colocalize almost exclusively with a mitochondrial marker in rat primary neuron, primary cardiomyocyte, and a murine hippocampal cell line. The colocalization of ERbeta and mitochondrial markers was identified by both fluorescence and confocal microscopy. No translocation of ERbeta into the nucleus on 17beta-estradiol treatment was seen by using immunocytochemistry. Immunoblotting of purified human heart mitochondria showed an intense signal of ERbeta, whereas no signals for nuclear and other organelle markers were found. Finally, purified human heart mitochondrial proteins were separated by SDS/PAGE. The 50,000-65,000 M(r) band was digested with trypsin and subjected to matrix-assisted laser desorption/ionization mass spectrometric analysis, which revealed seven tryptic fragments that matched with those of ERbeta. In summary, this study demonstrated that ERbeta is localized to mitochondria, suggesting a role for mitochondrial ERbeta in estrogen effects on this important organelle.
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              Ultrastructural localization of estrogen receptor beta immunoreactivity in the rat hippocampal formation.

              Several lines of evidence indicate that estrogen affects hippocampal synaptic plasticity through rapid nongenomic mechanisms, possibly by binding to plasma membrane estrogen receptors (ERs). We have previously shown that ERalpha immunoreactivity (ir) is in select interneuron nuclei and in several extranuclear locations, including dendritic spines and axon terminals, within the rat hippocampal formation (Milner et al., [2001] J Comp Neurol 429:355). The present study sought to determine the cellular and subcellular locations of ERbeta-ir. Coronal hippocampal sections from diestrus rats were immunolabeled with antibodies to ERbeta and examined by light and electron microscopy. By light microscopy, ERbeta-ir was primarily in the perikarya and proximal dendrites of pyramidal and granule cells. ERbeta-ir was also in a few nonprincipal cells and scattered nuclei in the ventral subiculum and CA3 region. Ultrastructural analysis revealed ERbeta-ir at several extranuclear sites in all hippocampal subregions. ERbeta-ir was affiliated with cytoplasmic organelles, especially endomembranes and mitochondria, and with plasma membranes primarily of principal cell perikarya and proximal dendrites. ERbeta-ir was in dendritic spines, many arising from pyramidal and granule cell dendrites. In both dendritic shafts and spines, ERbeta-ir was near the perisynaptic zone adjacent to synapses formed by unlabeled terminals. ERbeta-ir was in preterminal axons and axon terminals, associated with clusters of small, synaptic vesicles. ERbeta-labeled terminals formed both asymmetric and symmetric synapses with dendrites. ERbeta-ir also was detected in glial profiles. The cellular and subcellular localization of ERbeta-ir was generally similar to that of ERalpha, except that ERbeta was more extensively found at extranuclear sites. These results suggest that ERbeta may serve primarily as a nongenomic transducer of estrogen actions in the hippocampal formation. (c) 2005 Wiley-Liss, Inc.

                Author and article information

                S. Karger AG
                August 2006
                25 August 2006
                : 83
                : 2
                : 106-116
                Department of Biology, Georgia State University, Atlanta, Ga., USA
                94400 Neuroendocrinology 2006;83:106–116
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 2, References: 69, Pages: 11
                Original Paper


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