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), 17,20β-dihydroxy-4-pregnen-3-one (17,20β-P), and 17,20β,21-trihydroxy-4-pregnen-3-one (17,20β,21-P) remained low and unchanged in nonmaturing females, while 17β-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 T3profiles 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 E2increased first and peaked prior to FOM, whereas T peaked at the peripheral germinal vesicle (GV) stage. Plasma 17,20β-P and 17,20β,21-P increased dramatically at the GV breakdown (GVBD) stage. Plasma T4was unaffected by the GnRHa treatment, whereas T3decreased 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 E2and T elevations, and a late phase (yolk-globule coalescence, GVBD) associated with 17,20β-P and 17,20β,21-P elevation.

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