Endocrine correlates of reproductive development in the male tree-shrew (Tupaia belangeri) and the effects of infantile exposure to exogenous androgens.
The developmental life-history of tree-shrews conforms with the general primate pattern. Consequently, elucidation of the tree-shrew's neuroendocrine reproductive axis could shed light on the mechanisms that underlie human pubertal development. In the present study, we examined plasma gonadotropin concentrations in male tree-shrews from birth to sexual maturity, and related them to changes in the androgenic and gametogenic status of the testis. A hypogonadotropic infantile phase, during which a stable population of primordial cells is established, extended from birth to approximately Day 30. Following a short juvenile phase (Days 30-40), a pubertal phase of accelerated reproductive development was initiated between Days 40-55. At this time, FSH and LH levels rose and testosterone concentrations reached peak levels coincident with the descent of the testes, accelerated growth in the reproductive tract and the onset of spermatogenesis. To test whether this developmental peak in testosterone secretion is an important determinant in the normal onset of puberty, we exposed male tree-shrews prematurely to high circulating androgen levels for various periods and then examined the impact on key components of the developing reproductive axis. The testosterone implants failed to initiate spermatogenesis and the testes remained in an infantile state for the duration of the treatment, whereas implant removal led to the development of full spermatogenic activity. In both normal and experimental situations, low levels of FSH were associated with a lack of spermatogenic activity while the progression of germ cell development was precisely correlated with rising FSH levels. Taken together, these data establish a comprehensive picture of reproductive development in the male tree-shrew, and also provide support for the hypothesis that FSH plays a primary role in the initiation of spermatogenesis.
Collins
Peter M
PM
Department of Biological Sciences, University of California, Santa Barbara, CA 93106, USA. collins@lifesci.ucsb.edu
Tsang
Wai Ning
WN
Urbanski
Henryk F
HF
D000728:Androgens / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D004343:Drug Implants; D004703:Endocrine System / Q000187:drug effects* / Q000254:growth & development; D004822:Epididymis / Q000187:drug effects / Q000254:growth & development; D005640:Follicle Stimulating Hormone / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D009929:Organ Size / Q000187:drug effects; D011467:Prostate / Q000187:drug effects / Q000254:growth & development; D012669:Seminal Vesicles / Q000187:drug effects / Q000254:growth & development; D046468:Sexual Development / Q000187:drug effects*; D013737:Testis / Q000166:cytology / Q000187:drug effects / Q000254:growth & development; D013739:Testosterone / Q000097:blood; D014417:Tupaia / Q000097:blood / Q000254:growth & development / Q000502:physiology*
D000728:Androgens; D004343:Drug Implants; D013739:Testosterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone