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Biology of Reproduction 64, 1358-1365 (2001)
© 2001 Society for the Study of Reproduction, Inc.


Regular Article

Steroid Hormones Stimulate Gonadotrophs in Juvenile Male African Catfish (Clarias gariepinus)1

J.E.B. Cavaco3,a, J. van Baala, W. van Dijka, G.A.M. Hassinga, H.J. Th. Goosa, and R.W. Schulz2,a

a Research Group for Comparative Endocrinology, Faculty of Biology, Department of Developmental Biology, Utrecht University, 3584 CH Utrecht, The Netherlands

ABSTRACT

In juvenile African catfish (Clarias gariepinus), the pituitary LH content strongly increased after the beginning of spermatogonial proliferation. We hypothesized that a signal of testicular origin is involved in stimulating the gonadotrophs. We investigated the effects of castration and sex steroid treatment on gonadotrophs in juvenile males by quantifying LH production and release and LH subunit transcript levels and by examining gonadotroph morphology and proliferation. Castration reduced but did not abolish the maturation-associated elevation in pituitary LH content. Treatment with testosterone but not with 11-ketotestosterone, an otherwise potent androgen in fish, reversed the castration-induced decrease of pituitary LH levels. An increased pituitary LH content was accompanied by an increased number of cytologically mature gonadotrophs. However, no evidence was found for gonadotroph proliferation, so that quiescent gonadotrophs may have become activated. Although 11-ketotestosterone treatments had no effect in castrated males, this androgen attenuated gonadotroph activation in intact males. Because androgen production in juvenile catfish is downregulated by treatment with 11-ketotestosterone, its inhibitory effects on gonadotrophs in gonad-intact males may be due to suppression of Leydig cell testosterone production, which appears to be a limiting factor for the activation of catfish gonadotrophs. Aromatizable androgens may have opposite effects on fish (stimulatory) and mammalian (inhibitory) gonadotrophs.

FOOTNOTES

First decision: 18 October 2000.

1 This work was supported by grant BD/2603/93 from PRAXIS XXI J.N.I.C.T.–Portugal and by grant ENV4-CT97-0567 from the European Union. A preliminary report on part of the data was presented as a poster at the 18th European Conference for Comparative Endocrinologists, 10–14 September 1996, Rouen, France.

2 Correspondence: R.W. Schulz, Research Group Comparative Endocrinology, Faculty of Biology, Department of Developmental Biology, Utrecht University, Padualaan 8, 3584 CH Utrecht, The Netherlands. FAX: 31 30 2532837; r.w.schulz{at}bio.uu.nl

3 Current address: Molecular and Comparative Endocrinology, Universidade do Algarve-UCTRA, Centro de Ciências do Mar, Campus de Gambelas, P-8000-810 Faro, Portugal.




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