Prenatal exposure to perfluorooctanesulfonate in rat resulted in long-lasting changes of expression of synapsins and synaptophysin.

Both animal and human studies have demonstrated that exposure to chemical pollutants during critical developmental period causes adverse consequences later in life. In uterus, perfluorooctanesulfonate (PFOS) exposure has been known to cause developmental neurotoxicity, such as increased motor activity, reduced habitation and impaired cognitive function. The possible mechanism of the impaired cognitive function induced by prenatal PFOS exposure was evaluated in this study. Pregnant Sprague Dawley (SD) rats were given 0.1, 0.6, and 2.0 mg kg(-1) birth weight (bw) d(-1) by gavage from gestation day (GD) 0 to GD20. Control received 0.5% Tween-20 vehicle (4 ml kg(-1) bw d(-1)). PFOS concentration in hippocampus of offspring was observed on postnatal day (PND) 0 and PND21. The ultrastructure of hippocampus and the gene expression of synaptic vesicle associated proteins in offspring hippocampus, which were important for the neurotransmitter release, were investigated. The transmission electron photomicrographs of the offspring hippocampus from PFOS-treated maternal groups showed the ultrastructure of synapses was negatively affected. The offspring from PFOS-treated maternal groups also differed significantly from controls with respect to the expression of synaptic vesicle associated proteins. The mRNA levels of synapsin1 (Syn1), synapsin2 (Syn2), and synaptophysin (Syp) were decreased in treated groups either on PND0 or on PND21. However, the mRNA level of synapsin3 (Syn3) decreased in 0.6- and 2.0-mg kg(-1) group on PND0, and showed no significant difference among control group and all treated groups on PND21. These results indicate that the impairment of cognitive function induced by PFOS may be attributed to the lower mRNA levels of synaptic vesicle associated proteins and the change of synaptic ultrastructure in hippocampus.