Abstract
Gonadotropin-inhibitory hormone (GnIH) is a neurohormone that suppresses reproduction by acting at both the brain and pituitary levels. In addition to the brain, GnIH may also be produced in gonads and can regulate steroidogenesis and gametogenesis. However, the function of GnIH in gonadal physiology has received little attention in fish. The main objective of this study was to evaluate the effects of peripheral sbGnih-1 and sbGnih-2 implants on gonadal development and steroidogenesis during the reproductive cycle of male sea bass (Dicentrarchus labrax). Both Gnihs decreased testosterone (T) and 11-ketotestosterone (11-KT) plasma levels in November and December (early- and mid-spermatogenesis) but did not affect plasma levels of the progestin 17,20β-dihydroxy-4-pregnen-3-one (DHP). In February (spermiation), fish treated with sbGnih-1 and sbGnih-2 exhibited testicles with abundant type A spermatogonia and partial spermatogenesis. In addition, we determined the effects of peripheral Gnih implants on plasma follicle-stimulating hormone (Fsh) and luteinizing hormone (Lh) levels, as well as on brain and pituitary expression of the main reproductive hormone genes and their receptors during the spermiation period (February). Treatment with sbGnih-2 increased brain gnrh2, gnih, kiss1r and gnihr transcript levels. Whereas, both Gnihs decreased lhbeta expression and plasma Lh levels, and sbGnih-1 reduced plasmatic Fsh. Finally, through behavioral recording we showed that Gnih implanted animals exhibited a significant increase in diurnal activity from late spermatogenic to early spermiogenic stages. Our results indicate that Gnih may regulate the reproductive axis of sea bass acting not only on brain and pituitary hormones but also on gonadal physiology and behavior.
Highlights
As in other vertebrates, reproduction in fish is controlled by a complex system of endocrine, paracrine and autocrine regulatory signals that interact along the pineal-brain-pituitarygonadal axis [1,2,3,4]
Several studies have reported that gonadotropin-inhibitory hormone (GNIH) and/or its receptor (GNIHR) are expressed in gonads [21,22,23,24, 28] and are involved in the regulation of steroidogenesis in avian and mammalian species [23, 24, 26, 29]
Our findings revealed that prolonged sbGnih-1 and sbGnih-2 treatments during the reproductive cycle inhibited the testicular steroidogenesis (T and 11-KT but not DHP secretion) in particular reproductive stages, and that these effects were accompanied by evidence of partial and delayed spermatogenesis instead of complete, as observed in controls, as well as by a decrease in gonadotropin synthesis and release in the spermiation period (February)
Summary
Reproduction in fish is controlled by a complex system of endocrine, paracrine and autocrine regulatory signals that interact along the pineal-brain-pituitarygonadal axis [1,2,3,4]. Plasma levels of steroid hormones exhibit remarkable variations during male gonad maturation Androgens such as testosterone (T) and 11-ketotestosterone (11-KT) gradually increase their levels as spermatogenesis proceeds, decreasing at spermiation. Sexual steroids play a role in transducing the sexual status to the pituitary and brain via short and long regulatory feedback, respectively. The activation of these feedback mechanisms, with both positive and negative effects, depends on the phase of the development and of the reproductive cycle [12, 3]
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