Hyperactivity of basolateral amygdala mediates behavioral deficits in mice following exposure to bisphenol A and its analogue alternative. (January 2022)

• Record Type: Journal Article
• Authors: Hu, Fan; Liang, Weifeng; Zhang, Linke; Wang, Huan; Li, Zimu; Zhou, Yifeng
• Is Part Of: Chemosphere. Volume 287:Part 1(2022)
• Publication Date: 2022-01
• Subjects: Bisphenol A -- Bisphenol S -- Depression -- Anxiety -- Social behavior -- Basolateral amygdala; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2021.132044
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: Bisphenol A (BPA) is a known endocrine disruptor and has been gradually replaced in industrial applications by other bisphenols, such as bisphenol S (BPS). However, whether these analogues are any safer for the central nervous system remains elusive. Here, we investigated behavioral impairments in mice after BPA and BPS exposure from postnatal days 21–49 (P21~P49). Results showed that BPA (0.1 and 1 mg/kg/d) and BPS (1 mg/kg/d) impaired emotion and social interaction of mice, while low dose exposure (0.1 mg/kg/d) induced no observable changes on emotion in mice. The behavioral deficits were accompanied by hyperactivation of the basolateral amygdala (BLA), i.e., dose-dependent increase in neuronal firing rates and local field potential power. In addition, glutamate receptors were up-regulated in the BLA, showing the same activation trend after exposure to different doses of BPA and BPS. Taken together, these findings imply that BPA and BPS cause behavioral impairments in juvenile mice by disrupting local neuronal activation in the BLA. Although BPS exerted less adverse effects on mice than BPA at the low dose, it does not appear to be a safe alternative to BPA in regard to brain function after prolonged high-volume exposure. Graphical abstract: Image 1 Highlights: Juvenile BPA and BPS exposure cause behavioral impairments in mice. Hyperactivity in the BLA is involved in behavioral deficits. Glutamate receptor expression is up-regulated in the BLA of exposed mice.