PBDE-209 exposure damages learning and memory ability in rats potentially through increased autophagy and apoptosis in the hippocampus neuron

- Maternal exposure to PBDE-209 reduce offspring's learning and memory ability.
- Maternal exposure to PBDE-209 increases hippocampal neuron autophagy and apoptosis.
- PBDE-209 decrease neuron viability.
- Autophagy induced by PBDE-209 partly effect apoptosis induced by PBDE-209.
- Neurotoxicity of offspring may via increased autophagy and apoptosis.

This study is to investigate the neurotoxicity of PBDE-209 during pregnancy through autophagy and apoptosis in the fetal hippocampus neuron. The autophagy protein levels of LC3-II and Beclin-1 were significantly higher in hippocampus tissue and neuron, while P62 protein were lower. Apoptosis protein Cleaved Caspase-3 and Cleaved PARP was significantly higher in PBDE dose groups and BCL-2 levels in high PBDE dose groups were significantly lower. During the Morris water maze task, the escape latency times of high PBDE dose groups were significantly longer. PBDE-209-induced autophagy leads to neurons death and inhibition of autophagy reduce PBDE-209-induced apoptotic cell death. These results suggest that exposure of the PBDE-209 during pregnancy increases hippocampal autophagy, decrease neuron viability, and it partly effect apoptosis induced by PBDE-209. All that may contribute to the decline of learning and memory ability in the offspring.