In teleost fish, early sexual maturation is primarily regulated by the hypothalamic secretion of gonadotropin-releasing hormone (GnRH). Sustained pulsatile stimulation by GnRH results in elevated plasma estradiol (E ) levels, which in turn lead to a...
In teleost fish, early sexual maturation is primarily regulated by the hypothalamic secretion of gonadotropin-releasing hormone (GnRH). Sustained pulsatile stimulation by GnRH results in elevated plasma estradiol (E ) levels, which in turn lead to a reduction in the secretion of follicle-stimulating 2 hormone (FSH). Moreover, the stimulatory actions of GnRH on the hypothalamic–pituitary–gonadal (HPG) axis are antagonized by the modulation of dopamine (Da). In this study, under both in vitro and in vivo experimental conditions, we analyzed the mRNA expression levels of pituitary GnRH, FSH, and estrogen receptor alpha (ERα) during the sexual maturation process of olive flounder (Paralichthys olivaceus) to investigate the interaction between Da and E . In the in vitro experiment, 2 pituitary glands from immature females were cultured and treated with Da (2×10⁻⁹M to 2×10⁻⁷M) and E2 (2×10⁻⁷M) to evaluate their effects. In the in vivo experiment, Da and E2 were intraperitoneally injected at a dose of 5 mg/kg body weight, and the expression levels of GnRH, FSH, and ERα mRNA, along with the degree of gonadal development, were examined under various experimental conditions. Our results demonstrated that Da administration consistently suppressed the mRNA ex- pression of GnRH, FSH, and ERα, as well as gonadal development, across treatment groups. However, under in vivo conditions in which early sexual maturation was initially induced by E2 treatment fol-lowed by Da administration, FSH expression remained significantly suppressed, whereas GnRH ex-pression was not affected. These findings indicate that both Da and E2 act to downregulate GnRH and FSH gene expression in P. olivaceus, but that the inhibitory effect of Da on GnRH transcription is contingent upon the presence of E . Collectively, these results suggest that elevated estradiol levels 2 potentiate the suppressive effects of dopamine on both GnRH and FSH expression. In contrast, when E2 levels decline, ERα expression is reduced, thereby diminishing the inhibitory action of Da on GnRH secretion. Nevertheless, the suppression of FSH expression by Da appears to be maintained independently of E2 status.