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Kiss2 as a Regulator of Lh and Fsh Secretion via Paracrine/Autocrine Signaling in the Teleost Fish European Sea Bass (Dicentrarchus labrax)1
Author(s) -
F. Espigares,
Silvia Zanuy,
Ana Gómez
Publication year - 2015
Publication title -
biology of reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.366
H-Index - 180
eISSN - 1529-7268
pISSN - 0006-3363
DOI - 10.1095/biolreprod.115.131029
Subject(s) - kisspeptin , biology , medicine , endocrinology , gonadotropic cell , autocrine signalling , luteinizing hormone , paracrine signalling , gonadotropin , gonadotropin releasing hormone , neuropeptide , follicle stimulating hormone , pituitary gland , sea bass , hypothalamus , hormone , receptor , genetics , fishery , fish <actinopterygii>
Kisspeptins are key players in the neuroendocrine control of puberty and other reproductive processes in mammals. Several studies have demonstrated that the KISS/GPR54 system is expressed by gonadotrophs, but in vitro studies assessing the direct stimulatory effects of kisspeptin on gonadotropin secretion in the pituitary have provided conflicting results. In this study, we investigated whether kisspeptin directly influences the reproductive function of sea bass pituitary. First, the highly active peptides Kiss1-15 and Kiss2-12 were used to stimulate dispersed sea bass pituitary cells obtained from mature males. Our results show that, first, Kiss2-12 induced luteinizing hormone (Lh) and follicle-stimulating hormone (Fsh) release, whereas Kiss1-15 had no effect on gonadotropin secretion at full spermiation stage. Second, the distribution and nature of Kiss2 and its potential interactions with the gonadotropin-releasing hormone 1 (Gnrh1) system in the pituitary were analyzed using dual fluorescence immunohistochemistry. Kiss2 cells were found in the proximal pars distalis and colocalized with gonadotropin-immunoreactive cells. In summary, our results provide, for the first time in a teleost species, functional and neuroanatomical evidence that Kiss2 may act through different routes to directly modulate the activity of gonadotrophs, either as a hypophysiotropic neuropeptide or as an autocrine/paracrine factor.Peer Reviewe

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