Espermatogenesis

Hormonal regulation of spermatogenesis
Germ cell proliferation and survival depend heavily on
gonadotrophin-dependent mechanisms (McLachlan et al.
2002a), the subject of this review, although someaspects
appear to be gonadotrophin independent (Allan et al. 2004).
FSH exerts its biological effects via G protein-coupled FSH
receptors (FSHRs) found on the plasma membrane of the
Sertoli cells(Simoni et al. 1997, Heckert & Griswold 2002).
FSH signaling on Sertoli cells is known to activate at least
about five signaling pathways, such as cAMP and protein
kinase, MAP kinase, calcium,phosphatidylinositol 3-kinase,
and phospholipase A2 pathways (reviewed in Walker &
Cheng (2005)). These pathways eventually activate cAMPresponsive
element (CRE)-binding protein (CREB), and
thentranscribe downstream target genes of spermatogenesis.
Testosterone is synthesized by Leydig cells upon LH
stimulation (de Kretser et al. 1971, Wahlstrom et al. 1983).
Testosterone exerts itsbiological effects on spermatogenesis
via androgen receptors (ARs) that are localized in the Sertoli
cells (reviewed in Silva et al. (2002)). There is also evidence
for a non-genomic action of androgens, inwhich
testosterone elicits responses through secondary messengers
such as cAMP and signaling pathways different from classical
AR-mediated transcription (reviewed in Walker (2003)).
Cellularresponses following secondary messenger or
signaling pathways in Sertoli cells include the phosphorylation
of CREB and CRE modulator, and these transcription
factors have also been shown to beregulated by FSH (West
et al. 1994, Scobey et al. 2001). Despite common pathways
being activated by FSH and testosterone, some differences
exist, for example, testosterone does not up-regulate cAMPproduction in Sertoli cells (reviewed in Walker & Cheng
(2005)). In recent years, the characterization of the signaling
pathways regulated by FSH and testosterone has been an
important step toward the...