IMMUNOHISTOCHEMICAL DETECTION OF PROGESTIN RECEPTORS IN HYPOTHALAMIC BETA-ENDORPHIN AND SUBSTANCE-P NEURONS OF STEROID-TREATED MONKEYS

Progesterone (P) acts in the central nervous system to increase prolac tin secretion in estrogen (E)-primed female monkeys. beta-Endorphin (B E) and Substance P (SP) are two hypothalamic peptides which increase p rolactin secretion when administered to rats and monkeys. Studies were performed to determine if P acts on these two potential prolactin-rel easing systems. The presence of a nuclear steroid receptor defines the cell as a target for the cognate hormone, Therefore, the hypothalamic populations of BE and SP neurons were examined for the presence and r egulation of nuclear progestin receptors (PR) in spayed, E-treated (28 days) and E + P-treated monkeys (14 days E + 14 days E + P). Hypothal amic blocks were prepared after perfusion fixation with 4% paraformald ehyde. Cryosectioning(10 mu m) was followed by double immunocytochemis try (ICC) for PR (black nuclear stain) and either BE or SP (brown cyto plasmic stain). Sections were processed for ICC at 100- or 200-mu m in tervals through the hypothalamic block, Peptidergic neurons with and w ithout PR were counted in each section. The E + P-treated monkeys exhi bited a significant increase in serum prolactin. BE neurons were found only in the arcuate nucleus (ARC) and median eminence (ME). The coloc alization of BE and PR equaled 2% in spayed controls, 21% in the E-tre ated group and 25% in the E + P-treated group. SP neurons were located in a dorsomedial hypothalamic (DMH) subpopulation which extended caud ally under the mamillary nuclei and in a subpopulation located in the ARC and ME. Neither the DMH or submamillary SP neurons contained PR. T he percent colocalization of SP and PR in the ARC/ME equaled 5, 26 and 10% in the spayed, E- and E + P-treated groups, respectively. The dec rease in PR + SP colocalization with P treatment is probably due to a decrease in SP and not to a decrease in PR immunoreactivity. In summar y, E treatment induced PR in BE and SP neurons. Addition of P to the E treatment did not alter the expression of PR in BE neurons, but PR co localization decreased in SP neurons. Therefore, it is unlikely that S P neurons could transduce the action of P on prolactin secretion in pr imates, but BE neurons may play an intermediary role.