Primate spermatogenesis is distinguished by yet unidentified mechanisms to regulate its spermatogenetic activity. In contrast to the well documented hormonal regulators, the cellular events responsible for the regulation of the spermatogenesis has not been addressed. By using PGP 9.5-immunohistochemistry, our previous study demonstrated that the monkey spermatogonia are divided into two distinct sub-populations, i.e. cytoplasmic PGP 9.5-positive and cytoplasmic PGP 9.5-negative spermatogonia. By comparing the cytoplasmic expression of PGP 9.5 between the breeding and nonbreeding seasons of the Japanese monkey (Macaca fuscata) in association with PCNA labeling, the present study demonstrates that the cytoplasmic PGP 9.5-positive Ap spermatogonia significantly increases when the spermatogenetic activity declines in the nonbreeding season. An ultrastructural subcellular localization of PGP 9.5 suggests that the increase of the cytoplasmic PGP 9.5 expression is due to a liberation of PGP 9.5 molecule from the nucleus into the cytoplasm. The results provide a theoretical basis by which PGP 9.5 serves as a novel marker for spermatogonial subtypes, which will have further implications for future studies on spermatogenesis. The analysis using this novel marker suggests that the Ap spermatogonia is a key stage to regulate the amount of the sperm produced in response to the hormonal regulators, and the cytoplasmic liberation of PGP 9.5 may serve as a pivotal phenomenon that enables the fully restorable, transient suppression of spermatogenesis in primate.