Rationale

The endocrine control of testicular function is under investigation for many years. Once it became clear that LH/testosterone and FSH are the key factors in the control of the spermatogenic process, considerable efforts were spent in order to unravel the relative roles of testosterone and FSH for gametogenesis. A variety of experimental approaches was applied covering selective replacement of either hormone in hormone-deficient animal models, selective immunization against LH and FSH or their respective receptors, gene targeting of the reproductive hormones and their receptors, and selective elimination of testosterone-producing Leydig cells by toxicants.

The first edition ofthis bookwas published in 1990 followed by an update in 1998. It is interesting that major questions continue to remain an enigma, e.g. the precise mechanism of testosterone and FSH actions and how these hormones cooperate at the testicular level. On the other hand, significant new insights were gained, e.g. that, at least in primates, spermatogonia are the initial target of testosterone and FSH rather than meiotic cells or spermatids and that spermatid release (spermiation) is under endocrine control. Unlike a few years ago, when the relevance of FSH in adult spermatogenesis was questioned, it has become clear that FSH - probably more so than testosterone - is the key regulator of primate spermatogenesis.

The present chapter aims at providing a state-of-the-art review of our current understanding of the role of testosterone in spermatogenesis. Inevitably, we also review the role of FSH in spermatogenesis. A variety of species has been studied over the years and it became evident that certain nonhuman primate species are the most predictive preclinical animal model. Comparative analysis across species also revealed interesting insights such as the predominance of FSH for spermatoge-nesis in photoperiodic species and the observation that Leydig cells in marmosets normally operate with an "inactive" LH receptor.

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