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Effect of FSH on testicular morphology and spermatogenesis in gonadotrophin-deficient hypogonadal mice lacking androgen receptors

Division of Cell Sciences, University of Glasgow Veterinary School, Bearsden Road, Glasgow G61 1QH, UK
¹ Laboratory for Experimental Medicine and Endocrinology, Catholic University of Leuven, Herestraat 49, B-3000 Leuven, Belgium
² Department of Physiology, Anatomy and Genetics, University of Oxford, South Parks Road, Oxford OX1 3QX, UK

Correspondence should be addressed to P J O'Shaughnessy; Email: p.j.oshaughnessy{at}vet.gla.ac.uk

This is an Open Access article distributed under the terms of the Society for Reproduction and Fertility's Re-use Licence which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is roperly cited.

FSH and androgen act to stimulate and maintain spermatogenesis. FSH acts directly on the Sertoli cells to stimulate germ cell number and acts indirectly to increase androgen production by the Leydig cells. In order to differentiate between the direct effects of FSH on spermatogenesis and those mediated indirectly through androgen action, we have crossed hypogonadal (hpg) mice, which lack gonadotrophins, with mice lacking androgen receptors (AR) either ubiquitously (ARKO) or specifically on the Sertoli cells (SCARKO). These hpg.ARKO and hpg.SCARKO mice were treated with recombinant FSH for 7 days and testicular morphology and cell numbers were assessed. In untreated hpg and hpg.SCARKO mice, germ cell development was limited and did not progress beyond the pachytene stage. In hpg.ARKO mice, testes were smaller with fewer Sertoli cells and germ cells compared to hpg mice. Treatment with FSH had no effect on Sertoli cell number but significantly increased germ cell numbers in all groups. In hpg mice, FSH increased the numbers of spermatogonia and spermatocytes, and induced round spermatid formation. In hpg.SCARKO and hpg.ARKO mice, in contrast, only spermatogonial and spermatocyte numbers were increased with no formation of spermatids. Leydig cell numbers were increased by FSH in hpg and hpg.SCARKO mice but not in hpg.ARKO mice. Results show that in rodents 1) FSH acts to stimulate spermatogenesis through an increase in spermatogonial number and subsequent entry of these cells into meiosis, 2) FSH has no direct effect on the completion of meiosis and 3) FSH effects on Leydig cell number are mediated through interstitial ARs.

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				P. J. O'Shaughnessy, G. Verhoeven, K. De Gendt, A. Monteiro, and M. H. Abel Direct Action through the Sertoli Cells Is Essential for Androgen Stimulation of Spermatogenesis Endocrinology, May 1, 2010; 151(5): 2343 - 2348. [Abstract] [Full Text] [PDF]