In pikeperch,Sander lucioperca, aquaculture hormonal treatment is usually applied to synchronize ovulation. However, the effect ofdopamine (DA) receptor antagonists, in particular those blocking the D1 DA receptors, remains unknown. Thus, the aim of thepresent study was to investigate and compare the effects of D1 and D2 DA receptor antagonists on the sex-steroid production andreproductive performance of the species. Two experiments were performed during which mature pikeperch females were injectedwith different molecules: NaCl 0.9% (negative control) or human chorionic gonadotropin 500 IU/kg (positive control) in bothexperiments, metoclopramide (a D2 receptor antagonist; 4 mg/kg or 20 mg/kg) or SCH23390 (a D1 receptor antagonist; 0.8 mg/kgor 4 mg/kg) alone (experiment 1) or in combination with a salmon gonadotropin-releasing hormone analogue (sGnRHa at 25μg/kg;experiment 2). In experiment 2,fish were also injected with sGnRHa (25μg/kg) as positive control. Samplings of oocytes and bloodwere performed on the day of injection and after 24 h (both experiments), after 48 h (experiment 2) and at the time of ovulation(both experiments). In non-ovulatingfish, samplings were performed 7 days (experiment 1) or 14 days (experiment 2) afterinjection. In experiment 2, various zootechnical parameters of fertilized eggs were recorded (survival, hatching and malformationrates). The two antagonists alone were ineffective in inducing thefinal stages and regulating sex-steroid (testosterone,11 ketotestosterone, 17βestradiol and 17,20β-dihydroxy-4-pregnen-3-one) production. When administered with sGnRHa, bothSCH23390 and metoclopramide induced thefinal stages. However, only SCH23390 stimulated testosterone (4 mg/kg) and17βestradiol (0.8 mg/kg) production compared with sGnRHa alone. None of the treatments affected the survival, hatching ormalformation rates. This is thefirst report suggesting that in pikeperch the D1, but not the D2, DA receptor antagonist would beinvolved in the testosterone and 17βestradiol production as a potentiator of the sGnRHa effect.