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      Estrogen and Tamoxifen Differentially Regulate Beta-Endorphin and cFos Expression and Neuronal Colocalization in the Arcuate Nucleus of the Rat

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          Estrogen regulates hypothalamic gene expression, synthesis and release of the endogenous opioid peptide β-endorphin (βEND), although a consensus estrogen response element sequence has not been identified in the rat proopiomelanocortin (POMC) gene. POMC gene expression is also regulated by the activation of AP-1 promoter elements, which are known to be estrogen sensitive. The present studies examine whether estrogen modulates the hypothalamic POMC system through a non-classical mechanism involving AP-1 binding proteins such as cFos. Immunohistochemical double-labeling for βEND and cFos was used and immunoreactive (-ir) populations were quantified in the arcuate nucleus and periarcuate area across time using unbiased stereological methods. Ovariectomized rats were injected with 50 µg estradiol (E<sub>2</sub>), 500 µg tamoxifen citrate (TAM) or both (E<sub>2</sub>+TAM) and were perfused 1, 2, 4 or 48 h later. E<sub>2</sub> rapidly increased numbers of cFos-ir, βEND-ir and doubly-labeled cells after 4 h, and the number of βEND-ir cells remained high 48 h later, suggesting that the stimulatory effects of cFos on POMC in the hypothalamus persist after the cFos signal decays. Treatment with TAM alone did not affect the numbers of immunoreactive cells, although E<sub>2</sub>+TAM blocked the E<sub>2</sub>-mediated induction in all immunoreactive populations. Similar effects were seen at the transcriptional level. E<sub>2</sub> increased hypothalamic POMC mRNA after 4 h, while TAM treatment or coadministration of E<sub>2</sub>+TAM did not significantly change the levels of POMC mRNA. Cellular colocalization of βEND-ir and cFos-ir supports a possible intracellular co-regulation of these peptides by an estrogen-dependent mechanism within a subset of hypothalamic neurons. It does not, however, appear that E<sub>2</sub> acts directly through an AP-1 site within the POMC gene.

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          Most cited references 19

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          Comparative distribution of estrogen receptor-? and -? mRNA in the rat central nervous system

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            Differential Ligand Activation of Estrogen Receptors ER and ER at AP1 Sites

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              Tamoxifen activation of the estrogen receptor/AP-1 pathway: potential origin for the cell-specific estrogen-like effects of antiestrogens

               P. Webb (1995)

                Author and article information

                S. Karger AG
                November 2000
                05 December 2000
                : 72
                : 5
                : 293-305
                aDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, Md., and bFishberg Research Center in Neurobiology, Mount Sinai School of Medicine, New York, N.Y., USA
                54598 Neuroendocrinology 2000;72:293–305
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 6, References: 70, Pages: 13
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