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Role of the thyroid in ovarian maturation in the goldfish, Carassius auratus L Hurlburt, Mary E.


Thyroxine (T₄) administration by cholesterol pellet implantation, by immersion, or by feeding raised plasma T₄ levels of goldfish, Carassius auratus, above values of control fish (usually less than 1 μg/100 ml). Values for treated fish in the lower dosage groups generally fell between 1 and 4 μg/100 ml, while in the higher dosage groups plasma T₄ levels ranged from 5 to 16 μg/100 ml. Immersion was the most effective method of creating sustained physiological plasma T₄ elevations; both implantation and feeding are more suitable for flowing water systems where immersion is not feasible. Thyroxine treatment of maturing fish resulted in a depression of gonadotropin cell activity, while immersion of immature fish in the goiterogen, propylthiouracil, stimulated gonadotropin cell activity slightly; this effect was reversed by T₄ replacement therapy. T₄ administration to intact goldfish accelerated ovarian development in immature individuals, but had no apparent effect in mature fish. In hypophysectomized individuals, T₄ alone failed to initiate vitellogenesis or maintain yolky oocytes; the hormone did, however, augment the ovarian response to salmon gonadotropin (SG-G100) and ovine luteinizing hormone (LH) following pituitary ablation. Thyroxine treatment tended to increase relative liver weights in both intact and hypophysectomized fish, except when administered with LH. In the latter case, a combination of LH and T₄ prevented the usual liver hypertrophy after pituitary removal; either hormone alone, however, was ineffective, suggesting a synergistic action of the two hormones on liver function. In intact and hypophysectomized goldfish, SG-G100 and LH stimulated thyroid function, as measured by histological criteria and plasma T₄ analysis. The findings indicate that thyroid hormones act synergistically with gonadotropin to influence ovarian development in goldfish, and suggest that these effects are mediated, directly or indirectly, by a thyroxine-induced increase in ovarian sensitivity to gonadotropic stimulation. Thyroxine appears also to modulate gonadotropin production by a negative feedback on the hypothalamo-hypophysial axis; the physiological significance of this is, however, uncertain.

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