title: Search for progestin receptors (PR) in prolactin-releasing peptidergic neurons: oxytocin neurons lack PR, but respond to gonadal steroids in monkeys.
abstract: Progesterone (P) increases PRL secretion in estrogen (E)-primed primates, but not by a direct action on lactotropes. Oxytocin is one of several hypothalamic hormones that stimulate PRL secretion. This study was conducted to determine whether oxytocin neurons directly mediate the action of P on PRL secretion. Hypothalamic sections from steroid-manipulated macaques were double immunolabeled for oxytocin and progestin receptors (PR). In addition, serum levels of oxytocin were measured in steroid-treated macaques, and hypothalamic levels of oxytocin were measured in monkeys under various physiological conditions. E treatment (28 days) of spayed monkeys caused a significant increase in the number of PR-positive neurons in the preoptic area, ventromedial nucleus, arcuate nucleus, and median eminence. Addition of P to the E treatment for the last 14 of 28 days did not change the number of PR-positive neurons in these areas. The number of PR-positive neurons was low and was unchanged by steroid treatment in the supraoptic and rostral paraventricular nuclei. Oxytocin neurons rarely contained PR regardless of anatomical location, steroid treatment, or fixation protocol. Serum oxytocin levels increased with E treatment and increased further with supplemental P treatment. The rostral and medial basal hypothalamic content of oxytocin was significantly higher in macaques with mature gonads. In conclusion, oxytocin neurons do not express nuclear PR and probably do not transcriptionally respond to P. However, gonadal steroids apparently affect the production and release of oxytocin in vivo. Thus, it is possible that oxytocin neurons transduce the action of P on PRL secretion via stimulatory neurotransmission from another PR-containing neural system.
authors.affiliation: Division of Reproductive Sciences, Oregon Regional Primate Research Center, Beaverton 97006.
authors.forename: C L
authors.initials: CL
authors.lastname: Bethea
authors.forename: S G
authors.initials: SG
authors.lastname: Kohama
authors.forename: A A
authors.initials: AA
authors.lastname: Widmann
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000378:metabolism; D004343:Drug Implants; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D007016:Hypophysectomy; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D008252:Macaca fascicularis / Q000378:metabolism*; D008253:Macaca mulatta / Q000378:metabolism*; D008473:Median Eminence / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010052:Ovariectomy; D010121:Oxytocin / Q000378:metabolism; D011301:Preoptic Area / Q000378:metabolism; D011374:Progesterone / Q000494:pharmacology*; D011388:Prolactin / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000032:analysis / Q000378:metabolism*; D012016:Reference Values; D014697:Ventromedial Hypothalamic Nucleus / Q000378:metabolism
chemical_list: D004343:Drug Implants; D011980:Receptors, Progesterone; D011374:Progesterone; D004958:Estradiol; D010121:Oxytocin; D011388:Prolactin