Regulation of progestin receptors in raphe neurons of steroid-treated monkeys.

Progesterone increases prolactin secretion in estrogen-primed primates. This action is probably mediated through a neural mechanism since lactotropes do not have progestin receptors (PR). This laboratory recently reported localization of PR in serotonin neurons of female macaques. Since serotonin (5HT) is a putative prolactin stimulatory agent, it was of interest to examine the regulation of PR in this neural system. Spayed monkeys were treated with either (1) an empty silastic capsule; (2) an estrogen (E)-filled capsule for 28 days, or (3) an E-filled capsule for 28 days supplemented with a progesterone (P)-filled capsule for the last 14 of the 28 days. Pontine tissue blocks were obtained at autopsy and processed for immunocytochemistry. Adjacent sections (10 microns) throughout the extent of the raphe nuclei were immunostained for 5HT and PR. 5HT-positive and PR-positive cells were counted in the same area of the dorsal and ventral raphe of adjacent sections at 4 representative levels and the PR/5HT ratio was calculated. The number of 5HT-positive cells was not different in spayed, E- or E+P-treated groups. E-treatment significantly increased the number of PR-positive cells and the PR/5HT ratio in the dorsal and ventral raphe. Supplementary P treatment did not significantly decrease the PR/5HT ratio in these areas. This data suggests that E induces PR in the 5HT neuronal system and that the expression of PR is maintained in the presence of chronically elevated progestin. Thus, the expression of PR in the raphe is consistent with the manner in which P increases prolactin secretion in estrogen-primed primates.