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Gonadotrophs are the primary target cells for GnRH in the pituitary. However, during a limited period of neonatal life in the rat, lactotrophs and somatotrophs respond to GnRH as well. Also, in the adults of a number of teleost fishes (e.g. carp, goldfish, and tilapia but not trout), GnRH is a potent GH secretagogue. In studying hypophysiotrophic actions of the two forms of GnRH present in the African catfish (Clarias gariepinus), chicken GnRH-II ([His5,Trp7,Tyr8]GnRH; cGnRH-II) and catfish GnRH ([His5,Asn8]GnRH; cfGnRH), we have investigated the effects of GnRH on catfish gonadotrophs and somatotrophs. GnRH binding was examined by incubating dispersed pituitary cells attached to coverslips with 125I-labelled [d-Arg6,Trp7,Leu8,Pro9-Net]GnRH (sGnRHa), a salmon GnRH analogue with high affinity for the GnRH receptor. Following fixation and immunohistochemistry using antisera against catfish LH and GH, 125I-labelled sGnRHa was localised autoradiographically and silver grains were quantified on gonadotrophs and somatotrophs. Specific binding of 125I-labelled sGnRHa was restricted to gonadotrophs. Both cfGnRH and cGnRH-II dose-dependently inhibited 125I-labelled sGnRHa binding to gonadotrophs. To substantiate the localisation of functional GnRH receptors, the effects of cfGnRH and cGnRH-II on the cytosolic free calcium concentration ([Ca2+]i) were examined in Fura-2-loaded somatotrophs and gonadotrophs. GnRH-induced increases in [Ca2+]i appeared to be confined to gonadotrophs, in which both endogenous GnRHs caused a single and transient increase in [Ca2+]i. The amplitude of this [Ca2+]i transient depended on the GnRH dose and correlated well with the GnRHs' effect on LH release. In vivo experiments demonstrated that GnRH treatments which markedly elevated plasma LH levels had no effect on plasma GH levels, while a dopamine agonist (apomorphine) significantly elevated plasma GH levels. We conclude that the two endogenous forms of GnRH in the African catfish are not directly involved in the regulation of the release of GH, suggesting that GnRHs cannot be considered as GH secretagogues in teleosts in general.
Journal of Endocrinology (1997) 152, 437–446
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Abstract
The sensitivity of the pituitary to gonadotrophin-releasing hormone (GnRH) and that of the testis to gonadotrophin (GTH) was monitored in African catfish in vivo at different stages of pubertal development (20, 21, 24, 31, 39, 42 and 49 weeks of age). The fish were injected i.p. with chicken GnRH-II (cGnRH-II) or catfish GnRH (cfGnRH), their two endogenous GnRHs. Blood samples were collected to quantify LH-like GTH-II and three androgens 11-ketotestosterone (11-KT), testosterone and 11β-hydroxyandrostenedione (OHA). The testes of 20- and 21-week-old fish contained spermatogonia alone, or spermatogonia and spermatocytes, or – in a limited number of specimens – some spermatids as well. Spermatozoa were first observed in the testes of 24-week-old fish and became predominant as the fish attained full maturity (49 weeks of age). In 20- to 24-week-old fish, significantly elevated plasma GTH-II levels were only recorded after treatment with cGnRH-II. In 31- to 49-week-old fish, injection of both GnRHs led to increased plasma GTH-II levels, but cGnRH-II was always more effective than cfGnRH. Whereas basal GTH-II plasma levels hardly changed throughout the study, GnRH-stimulated levels increased with the age of the fish. Plasma concentrations of 11-KT were not different from controls in 20- and 21-week-old males despite their elevated GTH-II levels following injection of cGnRH-II. The first significant increase in levels of 11-KT after cGnRH-II treatment was observed in 24-week-old fish and, after cfGnRH treatment, in 39-week-old fish. Basal and GnRH-stimulated 11-KT plasma levels increased with the age of the fish. Basal and cGnRH-II-stimulated plasma levels of OHA and testosterone also increased with the age of the fish. However, the levels of OHA and testosterone were five- to tenfold lower than those of 11-KT and, except for OHA in the 49-week-old fish, no increases were recorded in the cfGnRH-injected fish. Our data show that at the beginning of spermatogenesis the pituitary gland is already sensitive to GnRH stimuli. However, sensitivity of the testicular steroidogenic system to GTH-II, sufficient to be reflected in consistently elevated androgen plasma levels, was not observed until 3–4 weeks later. The restricted testicular GTH-II responsiveness at the beginning of spermatogenesis may represent a limiting factor for further pubertal development.
Journal of Endocrinology (1994) 140, 265–273