Testicular steroidogenesis takes place almost exclusively in Leydig cells. Some metabolism of the androgens produced by Leydig cells takes place in seminiferous tubules, especially in the immature animal (e.g. aromatization and 5 alpha- reduction). Luteinizing hormone (LH) is the main tropic regulator of Leydig cell function, without which quantitatively important androgen production is not possible. LH acts through a receptor that belongs to the seven times cell membrane spanning, G protein associated, receptor family, and cyclic AMP is the main second messenger of its signal transduction. Information about the involvement of other signal transduction systems in LH action has also emerged recently. The action of LH is under manyfold modulation by other hormones (e.g. prolactin, growth hormone and insulin), growth factors and bioactive peptides. In this modulation, various paracrine and autocrine mechanisms play an important role. Seminiferous tubules influence the development and function of adjacent Leydig cells through several growth factors. When germ cells are damaged, Leydig cells in the vicinity proliferate faster. Leydig cell morphology also depends on the germ cell composition in the neighbouring seminiferous tubules, and certain stages of the seminiferous epithelial cycle increase the Leydig cell capacity to produce testosterone. Also negative modulation of Leydig cells by Sertoli/germinal cell derived factors has been demonstrated. However, the physiological importance of the paracrine and modulatory influences of the different hormones and growth factors still remains obscure since almost all information has so far been obtained from in vitro studies. In the study of testicular steroidogenesis, the main switch of the function, LH action, is well known whereas the role of the "in house" circuits of paracrine and autocrine regulation remain to be elucidated.