Perinatal exposure to nonylphenol impairs dendritic outgrowth of cerebellar Purkinje cells in progeny

Nonylphenol (NP) is a commercially produced nonionic surfactant that has become a global environmental pollutant due to poor biodegradability. Many studies have confirmed that NP has detrimental effects on the central nervous system. However, the damaging roles of NP on the cerebellum and the underlying mechanisms remain unclear. Therefore, we investigated the effects of perinatal exposure to NP on cerebellar Purkinje cell (PC) dendrites and explored the potential mechanism involved. The animal model of perinatal exposure to NP was established by orally administering dams with either corn oil or NP (10, 50, or 100 mg/kg) during pregnancy and lactation. Offspring subjected to NP exposure during pregnancy and lactation had shorter and fewer cerebellar PC dendritic branches in childhood (postnatal day (PND)21) and adulthood (PND80). Contrary to expectations, perinatal NP treatment increased phosphorylation of protein kinase C gamma on PND21, but not on PND80. However, perinatal exposure to NP decreased phosphorylation of stathmin and tropomyosin-related kinase B (TrkB), as well as the expression of brain derived neurotrophic factor (BDNF) in cerebellar PCs on PND21 and PND80. These results indicate that perinatal exposure to NP irreversibly inhibited dendritic growth of PCs in the cerebella of offspring. Furthermore, the irreversible damage to PC dendrites in the cerebella of offspring subjected to perinatal NP exposure may be due to increased stathmin activity mediated by BDNF-TrkB signaling. •Perinatal exposure to nonylphenol impairs dendritic outgrowth of Purkinje cell.•The impairment of dendritic outgrowth persists into adulthood.•BDNF/TrkB signaling may be involved in the irreversible impairment.