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Spermatogenesis and its endocrine regulation
Schulz, R.W.; Bogerd, J.; Goos, H.J.Th. (2000). Spermatogenesis and its endocrine regulation, in: Norberg, B. et al. (Ed.) Proceedings of the 6th International Symposium on the Reproductive Physiology of Fish, Bergen, Norway, July 4-9, 1999. pp. 225-232
In: Norberg, B. et al. (Ed.) (2000). Proceedings of the 6th International Symposium on the Reproductive Physiology of Fish, Bergen, Norway, July 4-9, 1999. Department of Fisheries and Marine Biology, University of Bergen: Bergen. ISBN 82-7461-048-2. 499 pp., more
In: International Symposium on the Reproductive Physiology of Fish. Museo Nacional de Ciencias Naturales, more

Available in Authors 
    VLIZ: Proceedings [4221]

Keyword
    Marine

Authors  Top 
  • Schulz, R.W.
  • Bogerd, J.
  • Goos, H.J.Th.

Abstract
    Spermatogenesis is the developmental process that provides spermatozoa. A self-renewing stem cell population produces spermatogonia, which proliferate during a specific number of mitotic cell cycles, before entering meiosis as primary spermatocytes. Secondary spermatocytes and then haploid spermatids emerge from the two meiotic cell cycles, carrying a recombined, unique set of genes. The final differentiation of spermatids into flagellated spermatozoa occurs during spermiogenesis. Germ cell survival and development depends on the continuous support by Sertoli cells; their number is limiting to sperm production. Spermatogenesis is regulated by extrinsic (endocrine and paracrine) and intrinsic (e.g. cell cycle regulation) cues. Spermatogenesis ceases upon androgen deprivation, hence the importance of steroidogenic gonadotropins regulating Leydig cell androgen production. Since androgen receptors have not been detected in germ cells but are present in Sertoli cells, the latter are considered to mediate androgen effects on germ cells. The molecular mode of action of androgens in spermatogenesis, however, remains poorly understood, and alternative paradigms should be tested. Androgens stimulate the proliferation of spermatogonia in eel, and indeed all subsequent steps of spermatogenesis. The development can be studied ex vivo, making this system a valuable experimental tool. Next to androgens, FSH is a major factor in the regulation of spermatogenesis in mammals. Sertoli cells express FSH receptors and mediate proliferative and anti-apoptotic signals to germ cells. In contrast to eel, spermatogonial proliferation in rodents responds to FSH rather than to androgens; in both cases, however, Sertoli cell-derived growth factors mediate the proliferative signal to the germ cells. While FSH increases the efficiency of spermatogenesis, it is not required for male fertility in mammals. Little is known about the role of FSH in fish spermatogenesis. It appears that the endocrine system mainly regulates the number of spermatogonial cells to be committed to maturation, and the somatic infrastructure needed for spermatogenesis. The timing of the successive developmental steps rather depends on autonomous systems operating in germ cells.

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