title: Endocrine profiles of female striped bass (Morone saxatilis) in captivity, during postvitellogenesis and induction of final oocyte maturation via controlled-release GnRHa-delivery systems.
abstract: Plasma levels of reproductive and thyroid hormones were measured in captive striped bass females during postvitellogenesis and the spawning period (March-June). Circulating gonadotropin II (GtH II), 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P), and 17,20beta, 21-trihydroxy-4-pregnen-3-one (17,20beta,21-P) remained low and unchanged in nonmaturing females, while 17beta-estradiol (E2) and testosterone (T) declined throughout postvitellogenesis. Plasma thyroxine (T4) declined significantly in mid-April, while triiodothyronine (T3) increased in mid-May. The only female that ovulated spontaneously had markedly different E2, T, and T3 profiles during postvitellogenesis, and had a surge in plasma GtH II during final oocyte maturation (FOM). The lack of a GtH II surge is presumably responsible for the absence of FOM, but earlier, and as of yet unknown, endocrine disruptions during postvitellogenesis may determine the female's ability to undergo FOM. Treatment of females with a gonadotropin-releasing hormone agonist (GnRHa)-delivery system induced FOM and ovulation within 3 and 10 days, respectively, and resulted in the production of fertile eggs. Plasma GtH II increased continually after GnRHa implantation, even in the presence of declining GnRHa plasma levels. Plasma E2 increased first and peaked prior to FOM, whereas T peaked at the peripheral germinal vesicle (GV) stage. Plasma 17,20beta-P and 17,20beta,21-P increased dramatically at the GV breakdown (GVBD) stage. Plasma T4 was unaffected by the GnRHa treatment, whereas T3 decreased after GnRHa implantation and remained low throughout FOM. Based on the observed hormonal profiles, FOM can be separated into an early phase (lipid-droplet coalescence, GV migration) associated with E2 and T elevations, and a late phase (yolk-globule coalescence, GVBD) associated with 17,20beta-P and 17,20beta,21-P elevation.
authors.affiliation: Columbus Center, University of Maryland Biotechnology Institute, 701 E. Pratt St., Baltimore, Maryland 21202, USA. DMylonas@cytanet.com.cy
authors.forename: C C
authors.initials: CC
authors.lastname: Mylonas
authors.forename: L C
authors.initials: LC
authors.lastname: Woods
authors.forename: P
authors.initials: P
authors.lastname: Thomas
authors.forename: Y
authors.initials: Y
authors.lastname: Zohar
mesh_terms: D000818:Animals; D000835:Animals, Wild; D001492:Bass / Q000502:physiology*; D003350:Cortodoxone / Q000031:analogs & derivatives / Q000097:blood; D004958:Estradiol / Q000097:blood; D005260:Female; D012739:Gonadal Steroid Hormones / Q000097:blood*; D007987:Gonadotropin-Releasing Hormone / Q000008:administration & dosage* / Q000819:agonists*; D006065:Gonadotropins, Pituitary / Q000097:blood; D006908:Hydroxyprogesterones / Q000097:blood; D009866:Oogenesis / Q000187:drug effects*; D013739:Testosterone / Q000097:blood; D013963:Thyroid Hormones / Q000097:blood*; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D014818:Vitellogenesis / Q000187:drug effects*
chemical_list: D012739:Gonadal Steroid Hormones; D006065:Gonadotropins, Pituitary; D006908:Hydroxyprogesterones; D013963:Thyroid Hormones; D014284:Triiodothyronine; C007433:17,20-dihydroxy-4-pregnen-3-one; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D004958:Estradiol; C051954:17,20,21-trihydroxy-4-pregnen-3-one; D013974:Thyroxine; D003350:Cortodoxone