Evidence for Intratesticular Factors Which Mediate the Response of Leydig Cells to Disruption of Spermatogenesis

Abstract

The traditional view of endocrine regulation of the testis placed the hypothalamic-pituitary unit in a commanding position such that the releasing and inhibiting hormones of the hypothalamus regulated the adenohypophysial secretion of luteinizing hormone (LH), follicle stimulating hormone (FSH), and prolactin (McCann, 1974; Neill, 1974). Studies of the action of these pituitary hormones led to the general acceptance that LH acts on the interstitial cells of Leydig to stimulate secretion of testosterone (Christensen, 1975). FSH was shown to bind to the seminiferous tubule, primarily the Sertoli cell, and to regulate the myriad of functions attributed to this cell (Means, 1977; Ritzen et al., 1981; Steinberger and Steinberger, 1977). The possibility remains that FSH may act upon additional testicular cell types; for example, testicular macrophages have been implicated (Yee and Hutson, 1985). Prolactin was shown to enhance the action of LH and was presumed to act at the level of the Leydig cell (Bartke et al., 1978). The role of prolactin in the maintenance of normal testicular function remains unclear. Negative feedback regulation of gonadal function is achieved by both steroidal and protein products of the testis acting on the hypothalamus and/or anterior pituitary (di Zerega and Sherins, 1981; Setchell, 1978).