Perinatal exposure to nonylphenol delayed myelination in offspring cerebellum.

As a stable environmental contaminant, nonylphenol (NP) has been shown to induce some neurological deficits in the cerebellum, although the underlying mechanism is still unknown. In the present study, we aimed to investigate the effects of perinatal exposure to NP on myelination, an important process essential for the intact cerebellar function, in the offspring cerebellum. Exposure to NP delayed the myelination in the offspring cerebellum during perinatal period. The myelination recovered in the cerebellum of offspring exposed to NP over time, and returned to normal in adulthood. In addition, perinatal exposure to NP reduced mature oligodendrocytes (myelin-forming glial cells) and increased astrocytes in the offspring cerebellum. BMP signaling is believed to negatively regulate oligodendrogliogenesis and myelination. In the present study, BMP4, p-Smad1/5, and ID4, key members of BMP signaling, were increased in the cerebellum of offspring exposed to NP. Taken together, these lines of evidence suggest that the activation of BMP signaling may underlie the decreased oligodendrogliogenesis and increased astrogliogenesis, and the consequent delay of myelination in the cerebellum of offspring perinatally exposed to NP.