Norstedt G, Mode A
Endocrinology. 1982 Aug;111(2):645-9. doi: 10.1210/endo-111-2-645.
The aim of the present study was to identify the primary sites of action of estrogens and androgens in the regulation of hepatic PRL receptors in the rat. Implantation of estradiol benzoate in the pituitary region of male rats caused a feminization (i.e. an increase) of PRL receptors to a concentration typical of that found in female rats. Estrogen implanted in the paraventricular region of male rats was less effective in causing such a feminization. Subcutaneous implantation of estrogen did not affect the PRL receptor concentration. It is concluded that estrogen induces PRL receptors via an action at the hypothalamo-pituitary level, possibly directly on the pituitary. The PRL receptor-suppressive action of sc injected testosterone was also exerted by the synthetic androgen R1881 (17 beta-hydroxy-17 alpha-methylestra-4,9,11-trien-3-one). However, anterior hypothalamic deafferentation rendered both male and female rats insensitive to this action of R1881. It is concluded that an intact hypothalamo-pituitary unit is required for the PRL receptor-suppressive action of R1991. It is possible that the site of action of androgens is in the rostral hypothalamus or in adjacent areas of the brain.
