Exposure to XXXX in the neonatal but not adult @entity19 results in synchronous spermatogenesis.

@entity72543 @entity19 @entity17777 @entity904 @entity15897 @entity57638 @entity1968 @entity46410
@entity1968 (RA) is required for germ cell differentiation, the regulation of which gives rise to a constant production of mature sperm. In testes from 3-day postpartum (dpp) RARE-hsplacZ @entity19 , periodic regions positive for beta-galactosidase activity were observed along the length of the seminiferous tubules. Periodicity was abolished by treatment of neonates with exogenous RA at 2 dpp. To assess the consequences, 2-dpp @entity19 were treated with RA, and the long- and short-term effects were assessed. Long-term effects of neonatal RA exposure included a delay in the appearance of advanced germ cells and the absence of a spermatogenic wave (synchronous spermatogenesis) in the adult. In contrast, RA exposure in @entity904 -sufficient adults did not result in synchronous spermatogenesis but rather induced apoptosis in a subset of spermatogonia. Shortly after (24 h) neonates were exposed, altered expression of known germ cell differentiation and the ( @entity46410 , @entity17777 , @entity57638 , and @entity72543 ) meiosis markers and an increase in the number of @entity46410 and @entity57638 immunopositive cells were observed relative to those of vehicle controls. However, 48 and 72 h after exposure, a significant reduction in the number of @entity46410 and @entity57638 immunopositive cells occurred. Immunohistochemical analysis of a marker for apoptosis demonstrated neonatal exposure resulted in increased germ cell apoptosis, as observed in the adult. Additionally, RA exposure resulted in increased @entity15897 expression of the RA-degrading enzyme. Thus, while RA treatment of neonatal and adult @entity19 resulted in apoptosis of spermatogonia, synchronous spermatogenesis occurred only after neonatal RA exposure.
