Seminiferous Cycle

Spermatogenesis is a unidirectional process with an intent to produce the most specialized cell type in the body, the sperm. However, spermatogenesis also has a cyclic nature. After a fixed species-dependent interval, called a cycle of the seminiferous epithelium, a certain area in the seminiferous tubule always has similar characteristics. In the seminiferous tubules, formation of cellular associations of constant composition is the outcome of synchronous development of different generations of spermatogenic cells. In living tissue and in a histological specimen, identification of these associations, called stages of the seminiferous epithelial cycle, is based primarily on the characteristics of the postmeiotic germ cells. The stages form segments and follow each other in a numerical order along the length of rodent seminiferous tubule to establish the wave of the seminiferous epithelium, whereas in human the stages follow a spiral form. Cyclical turnover of different cohorts of spermatogenic cells coincides with cyclic function of Sertoli cells, the somatic supporting cells. Sertoli cells transduce endocrine and paracrine stimuli into local regulation of spermatogenesis in a stage-dependent manner and are therefore the key regulators of the seminiferous cycle. The relationship of the seminiferous cycle and Sertoli cell cycle is complex but they are fully interdependent in the long run. While cyclic activity of Sertoli cells is needed for the onset of spermatogenesis in the prepubertal rodent testis, maintenance of the seminiferous cycle is taken care of by maturing germ cells that adjust the Sertoli cell "clock." However, cyclicity is an inherent property of Sertoli cells but, to be manifested fully, guidance from spermatogenic cells is likely needed. Retinoic acid (RA) has a key role at the onset of spermatogenic differentiation but testosterone and FSH (follicle-stimulating hormone) are required for the completion of quantitatively and qualitatively normal spermatogenesis. RA, testosterone and FSH all exert their effects on spermatogenesis in a stage-dependent manner. The mechanism behind the stage-dependent action of RA is the restriction of its availability, whereas seminiferous cycle-dependent receptor expression explains the stage-reliance of testosterone and FSH action.