Localization of estrogen receptor ?-immunoreactivity in astrocytes of the adult rat brain

Azcoitia, Íñigo; Sierra, Amanda; García‐Segura, Luis M.

doi:10.1002/(sici)1098-1136(199905)26:3<260::aid-glia7>3.0.co;2-r

Cited by 202 publications

(102 citation statements)

References 60 publications

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“…For visualization with DAB, alternating sections were labeled with rabbit polyclonal MC-20 (0.5 g/ml; Santa Cruz Biotechnology, Santa Cruz, CA) or mouse monoclonal 6F11 (1:50; Novocastra, Newcastle, UK), followed by species-specific biotinylated IgG (1:800; Vector Laboratories, Burlingame, CA), and visualized with DAB using an ABC kit (Vector Laboratories). Neither MC-20 (Azcoitia et al, 1999) nor 6F11 (Bevitt et al, 1997) cross-reacts with ER␤. Some sections were then dehydrated, cleared, and coverslipped under Eukitt for bright-field evaluation of nuclear and exatranuclear labeling.…”

Section: Methodsmentioning

confidence: 92%

Estrogen Mobilizes a Subset of Estrogen Receptor-α-Immunoreactive Vesicles in Inhibitory Presynaptic Boutons in Hippocampal CA1

Hart

Snyder²,

Smejkalová³

et al. 2007

J. Neurosci.

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Although the classical mechanism of estrogen action involves activation of nuclear transcription factor receptors, estrogen also has acute effects on neuronal signaling that occur too rapidly to involve gene expression. These rapid effects are likely to be mediated by extranuclear estrogen receptors associated with the plasma membrane and/or cytoplasmic organelles. Here we used a combination of serialsection electron microscopic immunocytochemistry, immunofluorescence, and Western blotting to show that estrogen receptor-␣ is associated with clusters of vesicles in perisomatic inhibitory boutons in hippocampal CA1 and that estrogen treatment mobilizes these vesicle clusters toward synapses. Estrogen receptor-␣ is present in approximately one-third of perisomatic inhibitory boutons, and specifically in those that express cholecystokinin, not parvalbumin. We also found a high degree of extranuclear estrogen receptor-␣ colocalization with neuropeptide Y. Our results suggest a novel mode of estrogen action in which a subset of vesicles within a specific population of inhibitory boutons responds directly to estrogen by moving toward synapses. The mobilization of these vesicles may influence acute effects of estrogen mediated by estrogen receptor-␣ signaling at inhibitory synapses.

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Section: Methodsmentioning

confidence: 92%

Estrogen Mobilizes a Subset of Estrogen Receptor-α-Immunoreactive Vesicles in Inhibitory Presynaptic Boutons in Hippocampal CA1

Hart

Snyder²,

Smejkalová³

et al. 2007

J. Neurosci.

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“…Localization and Role of Estrogen Receptors-In situ hybridization and immunohistochemical studies have revealed that both ER-α and ER-β are expressed in various regions of the hippocampus and prefrontal cortex in a variety of species [282][283][284][285][286]. In the female rat, mRNA for both estrogen receptors has been reported to be expressed in the hippocampus and cortex, with ER-β mRNA reportedly predominating over ER-α [282].…”

Section: Mechanisms Of Estrogen Regulation Of Synaptic Plasticitymentioning

confidence: 99%

Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications

et al. 2007

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Estrogen is an important hormone signal that regulates multiple tissues and functions in the body. This review focuses on the neurotrophic and neuroprotective actions of estrogen in the brain, with particular emphasis on estrogen actions in the hippocampus, cerebral cortex and striatum. Sex differences in the risk, onset and severity of neurodegenerative disease such as Alzheimer's disease, Parkinson's disease and stroke are well known, and the potential role of estrogen as a neuroprotective factor is discussed in this context. The review assimilates a complex literature that spans research in humans, non-human primates and rodent animal models and attempts to contrast and compare the findings across species where possible. Current controversies regarding the WHI (Women's Health Initiative) study, its ramifications, concerns and the new studies needed to address these concerns are also addressed. Signaling mechanisms underlying estrogen-induced neuroprotection and synaptic plasticity are reviewed, including the important concepts of genomic versus nongenomic mechanisms, types of estrogen receptor involved and their subcellular targeting, and implicated downstream signaling pathways and mediators. Finally, a multicellular mode of estrogen action in the regulation of neuronal survival and neurotrophism is discussed, as are potential future directions for the field.

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“…In the hippocampus, all enzymes of steroidogenesis are expressed, including aromatase, which converts testosterone to estradiol and represents the final step of estrogen synthesis (for review, see Azcoitia et al, 1999;Compagnone and Mellon, 2000;Garcia-Segura et al, 2001;Wehrenberg et al, 2001). A sixfold higher concentration of estradiol in the hippocampus than in plasma strongly indicates that estrogen synthesis takes place in the hippocampus (Hojo et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Hippocampal Synapses Depend on Hippocampal Estrogen Synthesis

et al. 2004

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Estrogens have been described to induce synaptogenesis in principal neurons of the hippocampus and have been shown to be synthesized and released by exactly these neurons. Here, we have focused on the significance of local estrogen synthesis on spine synapse formation and the synthesis of synaptic proteins. To this end, we reduced hippocampal estrogen synthesis in vitro with letrozole, a reversible nonsteroidal aromatase inhibitor. In hippocampal slice cultures, letrozole treatment resulted in a dose-dependent decrease of 17␤-estradiol as quantified by RIA. This was accompanied by a significant decrease in the density of spine synapses and in the number of presynaptic boutons. Quantitative immunohistochemistry revealed a downregulation of spinophilin, a marker of dendritic spines, and synaptophysin, a protein of presynaptic vesicles, in response to letrozole. Surprisingly, no increase in the density of spines, boutons, and synapses and in spinophilin expression was seen after application of estradiol to the medium of cultures that had not been treated with letrozole. However, synaptophysin expression was upregulated under these conditions. Our results point to an essential role of endogenous hippocampal estrogen synthesis in the maintenance of hippocampal spine synapses.

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Localization of estrogen receptor ?-immunoreactivity in astrocytes of the adult rat brain

Cited by 202 publications

References 60 publications

Estrogen Mobilizes a Subset of Estrogen Receptor-α-Immunoreactive Vesicles in Inhibitory Presynaptic Boutons in Hippocampal CA1

Estrogen Mobilizes a Subset of Estrogen Receptor-α-Immunoreactive Vesicles in Inhibitory Presynaptic Boutons in Hippocampal CA1

Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications

Hippocampal Synapses Depend on Hippocampal Estrogen Synthesis

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