REGULATION OF PROGESTIN RECEPTORS IN RAPHE NEURONS OF STEROID-TREATEDMONKEYS

Progesterone increases prolactin secretion in estrogen-primed primates . This action is probably mediated through a neural mechanism since la ctotropes do not have progestin receptors (PR). This laboratory recent ly 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 c apsule for 28 days supplemented with a progesterone (P)-filled capsule for the last 14 of the 28 days. Pontine tissue blocks were obtained a t autopsy and processed for immunocytochemistry. Adjacent sections (10 mu m) throughout the extent of the raphe nuclei were immunostained fo r 5HT and PR. 5HT-positive and PR-positive cells were counted in the s ame area of the dorsal and ventral raphe of adjacent sections at 4 rep resentative levels and the PR/5HT ratio was calculated. The number of 5HT-positive cells was not different in spayed, E- or E+P-treated grou ps. E-treatment significantly increased the number of PR-positive cell s 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 chroni cally elevated progestin. Thus, the expression of PR in the raphe is c onsistent with the manner in which P increases prolactin secretion in estrogen-primed primates.