Thyroid Hormone and Reproduction: Regulation of Estrogen Receptors in Goldfish Gonads

There is increasing evidence that thyroid hormones influence reproduction in vertebrates. However, little information is available on the mechanisms by which this happens. As a first step in determining these mechanisms, we test the hypothesis that the estrogen receptor subtypes (ER alpha, ER beta-1, and ER beta-2) are regulated by the thyroid hormone, (T-3), in the gonads of goldfish. All three subtypes were down-regulated by T-3 in the testis or ovary. We also found evidence that T-3 decreased pituitary gonadotropin expression and decreased transcript for gonadal aromatase. Collectively, it appears that T-3 acts to diminish estrogen signaling by (1) decreasing pituitary LH expression and thus steroidogenesis, (2) down-regulating gonadal aromatase expression and thus decreasing estrogen synthesis from androgens, and (3) decreasing sensitivity to estrogen by down-regulating the ER subtypes. Goldfish are seasonal breeders, spawning once a year, and thus have two distinct periods of growth: somatic and reproductive. Circulating thyroid hormone levels have been found to increase just after spawning. Therefore, we propose that this may be an endocrine mechanism that goldfish use to switch their energy expenditure from reproductive to growth efforts in the goldfish.