Abstract

In goldfish (Carassius auratus), pheromonal 17α,20β-dihydroxy-4-pregnen-3-one (17,20β-P) and spawning stimuli (interaction with a sexually active female releasing prostaglandin pheromone) both increase gonadotropin-II (GtH-II) and milt volume. In the goldfish pituitary, GtH-II release is stimulated by gonadotropin-releasing hormone (GnRH) and inhibited by dopamine (DA). In this study, we investigated the possibility that 17,20β-P and spawning stimuli act via separate neuroendocrine mechanisms by determining whether their effects on GtH-II could be selectively disrupted by injection of DA type-2 receptor (D-2) agonists (bromocryptine and LY171555) or a goldfish GnRH antagonist, [Ac-Δ3-Pro1, 4FD-Phe2,d-Trp3,6]-mGnRH (analog E). D-2 agonists blocked 17,20β-P-induced increases in GtH-II and milt volume but did not affect spawning-induced responses. GnRH antagonist blocked 17,20β-P-induced increases in GtH-II and milt volume, and spawning-induced GtH-II increase, but did not affect spawning-induced increase in milt volume. These results suggest that (1) pheromonal 17,20β-P and spawning stimuli increase GtH-II increase via distinct neuroendocrine mechanisms, (2) the effect of pheromonal 17,20β-P on increasing milt volume is GtH-II-dependent, and (3) the effect of spawning stimuli on increasing milt volume is GtH-II-independent.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call