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   <subfield code="a">Effect of steroid hormones and antihormones on hypothalamic beta-endorphin concentrations in intact and castrated female rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Andrea Genazzani, F. Petraglia, N. Mercuri, G. Brilli, A. Genazzani, M. Bergamaschi, B. DeRamundo, A. Volpe]</subfield>
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   <subfield code="a">The aim of the present study was to evaluate the effects of estrogens and androgens on hypothalamic beta-endorphin (β-EP) concentrations. Intact or castrated female rats were chronically (2 weeks) treated with estrogen (estradiol benzoate) and/or an-tiestrogens (clomiphene, cyclophenil or epimestrol), and with androgens (dihydrote-stosterone or dehydroepiandrosterone sulphate) and/or antiandrogen (cyproterone acetate). A group of rats treated with vehicle were studied as comparison. The β-EP concentrations were measured by radioimmunoassay on acidic extracts of rat hypothalami. The administration of clomiphene and cyclophenil significantly reduced hypothalamic β-EP concentrations in intact rats, while both drugs or estradiol benzoate increased the peptide concentration in castrated rats. Both intact and castrated rats treated with epimestrol showed hypothalamic β-EP concentrations higher than vehicle treated rats. The estradiol-induced increase of β-EP was not changed by the concomitant administration of an-tiestrogens. The administration of dihydrotes-tosterone significantly decreased β-EP concentrations in both intact and castrated female rats, while the treatment with dehydroepiandrosterone sulphate only slightly decreased β-EP levels in intact female rats. The cyproterone acetate-chronically treated rats showed higher β-EP concentrations than vehicle-treated rats and these changes were reversed by the concomitant addition of dihydrotestosterone or dehydroepiandrosterone sulphate. These results showed that estrogens play a positive role while androgens negatively influence the hypothalamic β-EP concentrations in female rats, supporting the view that central β-EP might be a target of gonadal steroid feedback signals.</subfield>
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   <subfield code="a">Italian Society of Endocrinology (SIE), 1990</subfield>
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   <subfield code="a">Estrogens</subfield>
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   <subfield code="t">Journal of Endocrinological Investigation</subfield>
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