The Sertoli cell is implicated centrally in spermatogenesis, organogenesis, male phenotypic development, and the hypothalamic-pituitary-gonadal axis. The cytoskeletal architecture of the Sertoli cell, as in many other cells, consists of actin filaments, intermediate filaments, and microtubules. The interaction of adjoining Sertoli cells with each other and with the basement membrane is crucially important to the function of the Sertoli cell: tight junctions and adherens junctions between Sertoli cells allow for the creation of an immunologically privileged space within the seminiferous tubule. This barrier, created by Sertoli cells and the basement membrane, is known as the blood-testis barrier. This chapter provides a brief discussion spermiogenesis and spermiation. Sertoli cells in adult mammals exist as a terminally differentiated, postmitotic population. Regulation of the Sertoli cell in its function as "nurse cell" for developing spermatogenic cells is obviously multifaceted and complex.

This chapter discusses the development of the adult population of Leydig cells from the stem cell precursor through the progenitor and immature Leydig cell stages. The morphogenetic events of early testis differentiation are controlled by the Sry (sex-determining region on the Y chromosome) gene. Lack of luteinizing hormone (LH) stimulation results in reduced steroidogenic enzyme activities and in Leydig cell atrophy. As men age, progressive decreases in serum concentrations of testosterone occur. Associated with these decreases are significant health consequences, including reduced sexual function, energy, muscle function, and bone density, and increased frailty and cognitive impairment. A number of hypotheses have been put forward over the years to explain changes that occur in aging cells, including late-onset gene expression, telomere shortening, gene modifications, changes in the immune system, and accumulated reactive oxygen-induced damage to DNA, lipids, and/or proteins.