Abstract Title:

Rapid effect of bisphenol A on glutamate-induced Cainflux in hippocampal neurons of rats.

Abstract Source:

Mol Cell Endocrinol. 2019 Jan 30. Epub 2019 Jan 30. PMID: 30707916

Abstract Author(s):

Xiaoyu Zhong, Jishui Li, Ziwei Zhuang, Qiaoqiao Shen, Kesheng Jiang, Yizhong Hu, Donghong Wu, Xiaohong Xu

Article Affiliation:

Xiaoyu Zhong


Intracellular Casignaling plays an essential role in synaptic plasticity. This study examined the effect of BPA on concentration of intracellular Ca([Ca]) by measuring fluorescence intensity of Cain hippocampal neurons in vitro. The results showed that BPA for 30 min exerted dose-dependently dual effects on glutamate-elevated [Ca]: BPA at 1-10 μM suppressed but at 1-100 nM enhanced glutamate-raised [Ca]. BPA-potentiated [Ca]was blocked by the antagonist of NMDA receptor and was eliminated by an estrogen-related receptor gamma (ERRγ) antagonist rather than an AR antagonist. Both inhibitors of MAPK/ERKs and MAPK/p38 blocked BPA-enhanced [Ca]. Co-treatment of BPA with 17β-Eor DHT eliminated the enhancement of 17β-E, DHT, and BPA in glutamate-elevated [Ca]. These results suggest that BPA at nanomole level rapidly enhances Cainflux through NMDA receptor by ERRγ-mediated MAPK/ERKs and MAPK/p38 signaling pathways. However, BPA antagonizes both estrogen and androgen enhancing NMDA receptor-mediated Cainflux in hippocampal neurons.

Study Type : Animal Study
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