Spermatogenesis is the series of processes occurring in the testis that results in the production of highly differentiated haploid spermatozoa from undifferentiated diploid spermatogonia. The purpose of this chapter is to review spermatogenesis and its hormonal regulation in higher primates; that is, species chiefly classified in the suborder Catarrhini.1 Although many basic concepts concerning spermatogenesis have resulted from experimental studies of rodent species, the suitability of these species for investigating all aspects of spermatogenesis and generalizing those results to primates, including man, must be considered with caution. This note of caution derives from observations indicating fundamental differences between the two phylo-genic orders in development, cellular events of spermatogenesis, and hormonal regu

1 Romer (1) defined the higher primates, Catarrhini, to comprise four families, namely, Anthropoidea, Cercopithecidae (Old-World Monkeys), Siimidae (manlike apes), and Hominidae (human). More recently, Hill (2) has revised the taxonomy of primates in his seminal work, The Primates, and has modified Romer's definition of higher primates into Platyrrhini (New-World primates) and Catarrhini (old-World primates). The Catarrhini are divided further into two superfamilies, Cercopithecidea (old-World monkeys) and Homonoidea (old-World apes and man). in addition, the old-World monkeys and the Hominoidea are more closely related to one another than either is related to the New-World monkeys.

From: Male Hypogonadism: Basic, Clinical, and Therapeutic Principles Edited by: S. J. Winters © Humana Press Inc., Totowa, NJ

lation of spermatogenesis. This should not be surprising. Although species of both orders have adapted successfully in many different environments, essentially spreading throughout the world, rodents' and primates' adaptive strategies are fundamentally different. Rodents have remained small animals throughout their evolutionary history, growing and maturing rapidly, usually in a few months, and reproducing frequently with large numbers of offspring in each litter. Rodents produce large populations of offspring, with diverse genotypes on which selective adaptation may operate (3). In contrast, primates have become larger during their evolutionary history, growing and maturing slowly usually for years, and reproducing infrequently, with only one or two offspring per pregnancy (4). Primates have produced small populations of individuals, with less genetic diversity on which selective adaptation may operate. Primates, perhaps because of their arboreal origin, have highly developed nervous systems, allowing these species to be more inquisitive, exploring new environmental niches, and learning rather than genetically adapting to novel habitats.

Although spermatogenesis is generally similar between these two orders, many details are remarkably different, and perhaps these differences accommodate the diverse strategies of adaptation. Three types of germ cells, namely, spermatogonia, spermato-cytes, and spermatids, and one somatic cell type, the Sertoli cells, that provide the structural support of and nutrients to the germ cells, comprise the epithelium of the seminiferous tubule of the mammalian testis. Perhaps the most remarkable difference between spermatogenesis in rodents and primates was identified in an early observation by a pioneer of reproductive biology. Smith (5) observed that surgical ablation of the pituitary gland of adult primates led to a more complete regression of the seminiferous epithelium than this surgery in rodents. In the former species, only Sertoli cells and stem spermatogonia remain after hypophysectomy, whereas in the rat, spermatogenesis was arrested during spermiogenesis (6-9). This difference is not likely to result from incomplete ablation of the rodent pituitary, as suggested by Smith (5), because chemical hypophysectomy in rats using a gonadotropin-releasing hormone-receptor (GnRH-R) antagonist, that dramatically suppresses gonadotropin secretion (10-12), similarly arrested spermatogenesis during spermiogenesis. Moreover, GnRH antagonist treatment of intact adult monkeys also causes regression of the seminiferous epithelium identical to that produced by hypophysectomy (10-12). In primates, the gonadotropic hormones are obligatory for development of differentiated spermatogonia, spermatocytes, and spermatids, whereas in rodents, a limited number of spermatids may be produced in the absence of a gonadotropin drive. The second major difference is that the mechanism of stem cell renewal is fundamentally dissimilar between rodents and higher primates (13). Third, the morphology of the various types of germ cells and the temporal relationships are more alike in the Cercopithecadea and Hominadea than other species (13).

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