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 prolactin secretion in estrogen (E)-primed female monkeys. beta-Endorphin (BE) and Substance P (SP) are two hypothalamic peptides which increase prolactin secretion when administered to rats and monkeys. Studies were performed to determine if P acts on these two potential prolactin-releasing 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 regulation of nuclear progestin receptors (PR) in spayed, E-treated (28 days) and E + P-treated monkeys (14 days E + 14 days E + P). Hypothalamic blocks were prepared after perfusion fixation with 4% paraformaldehyde. Cryosectioning (10 mu m) was followed by double immunocytochemistry (ICC) for PR (black nuclear stain) and either BE or SP (brown cytoplasmic stain). Sections were processed for ICC at 100- or 200-mu m intervals through the hypothalamic block. Peptidergic neurons with and without PR were counted in each section. The E + P-treated monkeys exhibited a significant increase in serum prolactin. BE neurons were found only in the arcuate nucleus (ARC) and median eminence (ME). The colocalization of BE and PR equaled 2% in spayed controls, 21% in the E-treated group and 25% in the E + P-treated group. SP neurons were located in a dorsomedial hypothalamic (DMH) subpopulation which extended caudally under the mamillary nuclei and in a subpopulation located in the ARC and ME. Neither the DMH or submamillary SP neurons contained PR. The 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 decrease in PR + SP colocalization with P treatment is probably due to a decrease in SP and not to a decrease in PR immunoreactivity. In summary, 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 colocalization decreased in SP neurons. Therefore, it is unlikely that SP neurons could transduce the action of P on prolactin secretion in primates, but BE neurons may play an intermediary role.
Bethea
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CL
Division of Reproductive Sciences, Oregon Regional Primate Reseach Center, Beaverton, OR 97006, USA.
Widmann
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AA
D000818:Animals; D004958:Estradiol / Q000097:blood / Q000494:pharmacology; D005260:Female; D000882:Haplorhini; D007031:Hypothalamus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007044:Hysterectomy; D007150:Immunohistochemistry; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010052:Ovariectomy; D011374:Progesterone / Q000097:blood / Q000494:pharmacology; D011388:Prolactin / Q000097:blood / Q000494:pharmacology; D011980:Receptors, Progesterone / Q000187:drug effects / Q000378:metabolism*; D013256:Steroids / Q000494:pharmacology*; D013373:Substance P / Q000502:physiology*; D001615:beta-Endorphin / Q000502:physiology*
D011980:Receptors, Progesterone; D013256:Steroids; D013373:Substance P; D011374:Progesterone; D004958:Estradiol; D001615:beta-Endorphin; D011388:Prolactin