Changes in plasma levels of 17 beta-estradiol after administration of an analogue of luteinizing hormone releasing hormone (LHRH-A) and pimozide in Diplectrum formosum (Teleostei: Serranidae)

Abstract

Gonadotropin secretion in teleosts is known to be stimulated by gonadotropin hormone releasing hormone (GnRH) and inhibited by dopamine. This study has investigated the effects of administration of pimozide (PIM) alone or in combination with an analogue of GnRH on plasma 17 beta-estradiol (17 beta-E) levels and the gonadosomatic index. Adult Diplectrum formosum were treated with a gonadotropin-releasing hormone analogue [des-Gly10 D-Ala6 Pro9 N-ethylamide (LHRH-A); 50, 70, and 100 ng/g body wt] alone or in combination with pimozide (PIM), a dopamine antagonist (0.5, 1.0, and 5.0 micrograms/g body wt). LHRH-A alone caused a dose-dependent increase in plasma 17 beta-E levels. A single injection of PIM (0.5 or 5.0 micrograms/g) 12 hr previous to a single injection of 100 ng/g body wt of LHRH-A increased 17 beta-E concentrations compared with fish receiving PIM alone; however, 1 microgram/g PIM did not change 17 beta-E plasma levels. Simultaneous administration of PIM (0.5, 1.0, and 5.0 micrograms/g body wt) and 100 ng/g body wt of LHRH-A at an interval of 12 hr (30% of the total dose of both PIM and LHRH-A was administered in the first injection and 70% in the second injection) significantly increased plasma 17 beta-E concentrations. The magnitude of this increase was at least threefold higher than those of fish receiving a single injection of PIM, 12 hr before a single injection of LHRH-A. LHRH-A or PIM alone or combined was ineffective in causing ovulation.