In nonprimates the spermatogonial compartment can be subdivided into (morphologically) undifferentiated spermatogonia and differentiating spermatogonia. Each cycle of the seminiferous epithelium the proliferative activity of the undifferentiated spermatogonia is stimulated, probably by factors secreted by Sertoli cells. Subsequently, during a period of active proliferation many Aal spermatogonia are formed. In the normal situation around epithelial stage III, proliferation is inhibited by the differentiating spermatogonia by way of a negative feedback system, probably involving a spermatogonial chalone. Then most of the Aal spermatogonia formed differentiate into Al spermatogonia. For this differentiation vitamin A, or factors secreted by Sertoli cells under the influence of vitamin A, is/are necessary. In the normal situation there is no regulation of the density of the undifferentiated spermatogonia. Different tubular areas can contain widely varying numbers of stem cells and other undifferentiated spermatogonia and consequently can produce widely varying numbers of Al spermatogonia. Only in extreme circumstances, such as after irradiation, the stem cells change the ratio between self-renewing and differentiating divisions in favor of self-renewal. Furthermore, in this situation the proliferation of the undifferentiated spermatogonia is not inhibited at epithelial stage III because of the lack of differentiating spermatogonia. Density regulation does take place during the development of the differentiating spermatogonia. In the chinese hamster it appeared that despite the variation in the numbers of Al spermatogonia produced in different areas, the density of the preleptotene spermatocytes was very much the same. It was found that the even distribution of spermatocytes in the epithelium was achieved by a density-dependent degeneration of differentiating spermatogonia in such a way that many of the latter cells degenerated in high density areas and only few or none in low density areas. In primates the undifferentiated spermatogonia can be subdivided into Ap and Ad spermatogonia. Both Ap and Ad spermatogonia can be seen to be topographically arranged in clones of 1 or 2n cells in situations in which their density is low. The Ad spermatogonia do not proliferate, but after cell loss these cells were found to transform into Ap spermatogonia that start to proliferate. The Ap spermatogonia only divide once every epithelial cycle, renewing themselves and giving rise to B spermatogonia. In the monkey the number of Ap spermatogonia could be increased by FSH treatment. Hence, there may be a correlation between FSH levels and the numbers of Ap spermatogonia. Fu