title: Physiological consequences of social descent: studies in Astatotilapia burtoni.
abstract: In many species, social interactions regulate reproductive capacity, although the exact mechanisms of such regulation are unclear. Since social stress is often related to reproductive regulation, we measured the physiological signatures of change in reproductive state as they relate to short-term stress and the stress hormone cortisol. We used an African cichlid fish, Astatotilapia burtoni, with two distinct, reversible male phenotypes: dominant (territorial, T) males that are larger, more brightly colored, more aggressive, and reproductively competent and non-dominant males (non-territorial, NT) that are smaller, camouflage colored, and have regressed gonads. Male status, and hence reproductive competence, depends on social experience in this system. Specifically, if a T male is placed among larger male fish, it quickly becomes NT in behavior and coloration, but complete regression of its reproductive axis takes ca. 3 weeks (White et al. 2002). Reproduction in all vertebrates is controlled by the hypothalamic-pituitary-gonadal axis in which the key signaling molecule from the brain to the pituitary is GnRH1. Here, we subjected T males to territory loss, a social manipulation which results in status descent. We measured the effects of this status change in levels of circulating cortisol and testosterone as well as mRNA levels of GnRH1 and GnRH receptor-1 (GnRH-R1) in the brain and pituitary, respectively. Following short-term social suppression (4 h), no change was observed in plasma cortisol level, GnRH1 mRNA expression, GnRH-R1 mRNA expression, or plasma testosterone level. However, following a somewhat longer social suppression (24 h), cortisol and GnRH1 mRNA levels were significantly increased, and testosterone levels were significantly decreased. These results suggest that in the short run, deposed T males essentially mount a neural 'defense' against loss of status.
authors.affiliation: Program in Human Biology, Stanford University, CA 94305-5020, USA.
authors.forename: Victoria N
authors.initials: VN
authors.lastname: Parikh
authors.forename: Tricia
authors.initials: T
authors.lastname: Clement
authors.forename: Russell D
authors.initials: RD
authors.lastname: Fernald
mesh_terms: D000818:Animals; D001923:Brain Chemistry; D023681:Cichlids / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D015870:Gene Expression; D007987:Gonadotropin-Releasing Hormone / Q000235:genetics; D006608:Hierarchy, Social; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D010902:Pituitary Gland / Q000737:chemistry; D012333:RNA, Messenger / Q000032:analysis; D012098:Reproduction / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013312:Stress, Physiological / Q000097:blood*; D013739:Testosterone / Q000097:blood; D013997:Time Factors
chemical_list: D012333:RNA, Messenger; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D006854:Hydrocortisone