Testicular steroidogenesis and locomotor activity are also regulated by gonadotropin-inhibitory hormone in the male European sea bass.

Abstract

Gonadotropin-inhibitory hormone (GnIH) suppresses reproduction in several vertebrate species by acting at both the brain and pituitary levels. New evidences obtained in birds and mammals suggest that, in addition to the brain, GnIH may also be produced in testis and ovary and can regulate gonadal steroidogenesis and gametogenesis. Sex steroids are essential for gonadal function and cyclicity and play a key role in referring the sexual status to the brain and pituitary. However, the function of GnIH in gonadal physiology has received scanty attention in fish. One of the aims of this study was to evaluate the effects of peripheral sbGnIH-1 and sbGnIH-2 implants on gonadal development and steroidogenesis along the reproductive cycle of male sea bass. Implants of sbGnIH-1 and sbGnIH-2 peptides did not affect plasma levels of the maturation-inducing steroid 17,20¿-dihydroxy-4-pregnen-3-one. Although similar profiles of plasma testosterone (T) and 11-kestostestosterone (11-KT) were observed in controls and GnIH-implanted animals, with a peak in January, both GnIHs decreased T and 11-KT plasma levels in November and December. In February, control fish only exhibited late meiotic and full spermiogenic testicles containing mostly sperm. In contrast, both sbGnIH-1 and sbGnIH-2 treated fish also exhibited a significant percentage of testicles containing abundant type A spermatogonia and partial spermatogenesis. In addition, we determined the effects of peripheral GnIH implants on plasma FSH and LH levels, as well as on brain and pituitary expression of reproductive hormones genes (gnrh1, gnrh2, gnrh3, kiss1, kiss2, gnih, lhbeta, fshbeta) and their receptors (gnrhr II-1a, gnrhr II-2b, kiss1r, kiss2r and gnihr) at the spawning period (February). Treatment with sbGnIH-2 increased brain gnrh2, gnih, kiss1r and gnihr transcripts. Moreover, both sbGnIH-1 and sbGnIH-2 treatments decreased lhbeta expression and plasma LH levels, but only sbGnIH-1 reduced plasmatic FSH. Finally, we have shown that both GnIHs prevented the characteristic increase in nocturnalism observed in sea bass during the reproductive season. Taken together, our results indicate that GnIH may regulate the reproductive axis of sea bass acting not only at the brain and pituitary level but also on gonadal physiology and reproductive behaviour.