Publisher Summary This chapter discusses the influence of the Leydig cell on seminiferous tubule function and the influence of the tubule on the Leydig cells. For over 40 years, the two compartments of the testis, the seminiferous tubules and Leydig cells, were portrayed as independent functional units. Follicle stimulating hormone (FSH) was designated as the stimulus for spermatogenesis and luteinizing hormone (LH) as the factor controlling Leydig cell function, these requirements being identified in experiments involving hypophysectomy of rats. However, over 15 years ago, it was demonstrated that LH influenced spermatogenesis through the secretion of testosterone by the Leydig cells, thereby establishing a paracrine component to the physiology of testicular function. This role was even demonstrated by the observation that seminiferous tubules immediately in the vicinity of Leydig cell testosterone—producing adenomas in prepubertal boys showed active spermatogenesis, whereas those distantly placed remained as seminiferous cords. More recently, interest in local control mechanisms within the testis has increased, stimulated by two groups of observations that indicate that the seminiferous tubules can significantly influence Leydig cell function. The models of spermatogenic damage in the rat, showed that the function and structure of the Leydig cells in these states were altered, indicating that the agents used affected both spermatogenesis and the Leydig cells or alternatively, that the state of the tubule influenced the Leydig cells.
