title: Social suppression of cortisol in female marmosets: role of luteinizing hormone/chorionic gonadotropin.
abstract: Behaviorally subordinate female common marmosets (Callithrix jacchus) undergo suppression of ovulation and chronic reductions in basal plasma cortisol concentrations. Indirect evidence suggests that hypophyseal chorionic gonadotropin (CG; the major pituitary luteinizing gonadotropin in marmosets) may elevate cortisol concentrations in female marmosets, and therefore that social suppression of CG may contribute to diminution of cortisol in subordinates. To test this hypothesis, we determined whether pharmacological inhibition of pituitary CG release decreases basal and adrenocorticotropin (ACTH)-stimulated cortisol secretion. We characterized cortisol and reproductive hormone concentrations in six ovary-intact and six ovariectomized marmosets during long-term treatment with leuprolide acetate, a gonadotropin-releasing hormone (GnRH) agonist, and vehicle. Leuprolide suppressed basal plasma CG concentrations, abolished the CG response to exogenous GnRH, and, in intact animals, blocked ovarian cyclicity. During treatment with vehicle, plasma cortisol concentrations were elevated during the periovulatory phase in intact females, compared to the follicular phase, the luteal phase, and ovariectomized females. Leuprolide suppressed basal cortisol concentrations of intact females as compared to the periovulatory phase, but did not affect basal cortisol in ovariectomized animals and did not alter responses to exogenous ACTH. These findings suggest that elevations in circulating CG concentrations are associated with elevated cortisol concentrations in female marmosets, and that this relationship requires simultaneous increases in ovarian hormones that occur only during the periovulatory period. Thus, suppression of CG release in anovulatory subordinate females may not play an important role in socially induced diminution of cortisol.
authors.affiliation: Department of Biology, University of California-Riverside, Riverside, CA 92521, USA. saltzman@ucr.edu
authors.forename: Wendy
authors.initials: W
authors.lastname: Saltzman
authors.forename: Brynn K
authors.initials: BK
authors.lastname: Hogan
authors.forename: Brian M
authors.initials: BM
authors.lastname: Horman
authors.forename: David H
authors.initials: DH
authors.lastname: Abbott
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D002144:Callithrix / Q000502:physiology* / Q000523:psychology*; D006063:Chorionic Gonadotropin / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000031:analogs & derivatives / Q000652:urine; D005260:Female; D006854:Hydrocortisone / Q000097:blood; D016729:Leuprolide / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000378:metabolism*; D008297:Male; D010053:Ovary / Q000187:drug effects / Q000378:metabolism; D010060:Ovulation / Q000502:physiology / Q000523:psychology; D011374:Progesterone / Q000097:blood; D012930:Social Dominance
chemical_list: D006063:Chorionic Gonadotropin; C031555:estradiol sulfate; D011374:Progesterone; D004958:Estradiol; D000324:Adrenocorticotropic Hormone; D007986:Luteinizing Hormone; D016729:Leuprolide; D006854:Hydrocortisone