Abstract
AbstractMaturing female rainbow trout were injected two times with gonadotropin‐releasing hormone analogue (GnRHa) or once with triiodothyronine (T3) alone or in combination. GnRHa treatment caused ovulation within 10 days after the second injection. T3 treatment caused a severalfold increase in blood plasma T3 concentrations and increased the ovulatory response to GnRHa. Ninety percent of the fish injected with both T3 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 (E2) levels decreased between the time of the first injection and the time of spawning. GnRHa decreased TA levels and increased thyroxine and T3 levels, but did not affect either E2 or DHP concentration in the blood plasma of the fish at the time of spawning. To investigate the mechanism of action of T3 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 T3. The lower concentrations of T3 (0.5 to 50 ng/ml) potentiated oocyte maturation (germinal vesicle breakdown [GVBD]) in response to SG‐G100. The highest concentration of T3 inhibited GVBD. T3 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.
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