Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5560939 | NeuroToxicology | 2017 | 9 Pages |
â¢Both male and female neonatal rats were exposed to BDE 209.â¢Exposure to BDE 209 elicited evident learning and memory deficits in adult rats.â¢SNARE-related proteins were significantly decreased in the rats' hippocampi.â¢There were no obvious sex differences in the effects or alterations.
Polybrominated diphenyl ethers (PBDEs) are a class of flame retardants. While the mechanism remains unknown, the potential neurotoxic effects of PBDEs remain a relevant issue. In the present study, neonatal Sprague-Dawley rats of both sexes were administered BDE 209 (1, 10, or 20Â mg/kg body weight) or peanut oil once daily from postnatal day (PND) 5 to PND 10. We examined the spatial learning and memory by Morris water maze and the working and reference memory by eight-arm radial maze in the stage of adulthood. Compared with controls, significantly longer escape latencies and fewer platform-crossings in the Morris water maze were observed in rats exposed to 1, 10, and 20Â mg/kg BDE 209, and these effects were dose-dependent. Significantly higher working and reference memory error rates in the eight-arm radial maze were also observed in rats exposed to 10 and 20Â mg/kg BDE 209. Furthermore, we detected the mRNA and protein expressions of hippocampal synaptobrevin 2, syntaxin 1A, Synaptosome Associated Protein 25 (SNAP-25), and synaptophysin using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blot methods. Compared with controls, the mRNA expressions of synaptobrevin 2, syntaxin 1A, SNAP-25, and synaptophysin were significantly decreased in the hippocampi of rats exposed to 1, 10, and 20âmg/kg BDE 209, and the protein expressions of synaptobrevin 2 and SNAP-25 were significantly decreased in the hippocampi of rats exposed to 10 and 20âmg/kg BDE 209, while syntaxin 1A and synaptophysin were significantly decreased in rats exposed to 1, 10, and 20âmg/kg BDE 209. Alterations that may be involved in the learning and memory deficits induced by BDE 209 reveal the possibility of synapse loss.