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Regulation of Prolactin Messenger Ribonucleic Acid Levels by Estradiol and Dihydrotestosterone as Evaluated by in situ Hybridization Performed on Implanted Pituitary Glands and Anterior Pituitary Cells in Culture in the Male Rat
Author(s) -
Tong Yiai,
Veilleux Raymonde,
Pelletier Georges
Publication year - 1992
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1992.tb00180.x
Subject(s) - medicine , endocrinology , prolactin , anterior pituitary , dihydrotestosterone , pituitary gland , hypothalamus , messenger rna , biology , prolactin cell , estrogen , in situ hybridization , stimulation , hormone , chemistry , androgen , gene , biochemistry
We have recently demonstrated that 17ß‐estradiol (E 2 ) administration increases protactin (PRL) mRNA levels in the male rat anterior pituitary gland and that this stimulatory effect is partially inhibited by concomitant administration of dihydrotestosterone. In order to gain more information about the site(s) of action of E 2 and dihydrotestosterone on PRL gene expression, we have studied the effects of these two hormones in pituitaries implanted under the kidney capsule as well as in anterior pituitary cells in culture. In implanted pituitaries, PRL mRNA levels were increased by 90% as compared to values obtained in the stalk‐connected pituitaries from the same animals. Administration of E 2 induced a further increase of PRL mRNA levels in implanted pituitaries, while dihydrotestosterone did not produce any change in animals which had been treated or not with E 2 . In anterior pituitary cells in culture, addition of E 2 to the culture medium resulted in a 60% increase of PRL mRNA levels over control values. Supplementation with dihydrotestosterone did not induce any variation in the concentration of PRL mRNA in cells which were treated or not with E 2 . These results indicate that E 2 exerts a direct action on PRL cells at the pituitary level and strongly support the key role of the hypothalamus in the inhibitory effect of androgens on estrogen‐induced stimulation of PRL mRNA in the male rat pituitary.