Although molecular mechanisms underlying steroid effects on GnRH and dopamine receptors are well documented in mammals, little is known in fish. Herein, we describe the expression of pituitary GnRH and dopamine receptors relative to gonadotropin expression and release. We exposed female tilapia to graded doses of estradiol or 17alpha,20beta-dihydroxy-4-pregnen-3-one (DHP) in vitro, and of estradiol in vivo, and determined mRNA levels of gnrhr1, gnrhr3, drd2, lhb, and fshb by real-time PCR. We also determined gonadotropin levels using specific ELISAs. Exposure to low doses of estradiol caused increased gnrhr3 mRNA levels in vivo and in vitro, probably related to positive feedback on FSH release. Increasing concentrations of estradiol resulted in increased drd2 mRNA levels in vivo and in vitro, inhibition of LH and FSH release, and inhibition of lhb mRNA levels in vivo, possibly related to negative feedback. At high doses of estradiol, FSH release increased in preparation for a new generation of follicles. Exposure to nanomolar doses of DHP resulted in increased drd2 mRNA levels, probably related to negative feedback on LH release. A decrease in drd2 levels at the micromolar range of DHP (concomitant with increased gnrhr3 and fshb mRNA levels) may be related to tine recruitment of a new generation of oocytes. Exposure to DHP also resulted in increased lhb mRNA levels toward final oocyte maturation. Salmon GnRH analog (sGnRHa) increased mRNA levels of gnrh1 and gnrh3; when combined with DHP, sGnRHa synergistically increased expression of gnrh3 only. These results emphasize the role of sex steroids on positive and negative feedbacks controlling the reproductive cycle.
- Gonadotropin-releasing hormone receptor