Thyroid hormones in trout reproduction: Enhancement of gonadotropin‐releasing hormone analogue and partially purified salmon gonadotropin‐induced ovarian maturation in vivo and in vitro

Maturing female rainbow trout were injected two times with gonadotropin‐releasing hormone analogue (GnRHa) or once with triiodothyronine (T 3 ) alone or in combination. GnRHa treatment caused ovulation within 10 days after the second injection. T 3 treatment caused a severalfold increase in blood plasma T 3 concentrations and increased the ovulatory response to GnRHa. Ninety percent of the fish injected with both T 3 and GnRHa ovulated within 3 days after the second GnRHa injection, as opposed to 50% of the fish injected only with GnRHa, or 25% of the controls. In all groups total androgen (TA) and 17α‐20β‐dihydroxy‐4‐pregnen‐3‐one (DHP) levels increased and estradiol (E 2 ) levels decreased between the time of the first injection and the time of spawning. GnRHa decreased TA levels and increased thyroxine and T 3 levels, but did not affect either E 2 or DHP concentration in the blood plasma of the fish at the time of spawning. To investigate the mechanism of action of T 3 on trout maturation, oocytes within intact follicles were cultured in the presence of various concentrations (0.1 to 1,000 ng/ml) of partially purified salmon gonadotropin (SG‐G100) with or without various concentrations (0.5 to 500 ng/ml) of T 3 . The lower concentrations of T 3 (0.5 to 50 ng/ml) potentiated oocyte maturation (germinal vesicle breakdown [GVBD]) in response to SG‐G100. The highest concentration of T 3 inhibited GVBD. T 3 was effective in increasing GVBD only at the lowest concentration of SG‐G100 (10 ng/ml) that was effective in stimulating GVBD. The percentage of oocytes that had undergone GVBD was positively correlated with the concentration of DHP in the culture medium. These results suggest that thyroid hormones may influence final maturation of trout by potentiating the steroidogenic responses of the ovary to gonadotropin.