Bisphenol-A Exposure during Gestation and Lactation Causes Visual Perception Deficits in Rat Pups Following a Decrease in Interleukin 1β Expression in the Primary Visual Cortex. (10th May 2020)

• Record Type: Journal Article
• Authors: Hu, Fan; Zhang, Linke; Li, Tingting; Wang, Huan; Liang, Weifeng; Zhou, Yifeng
• Is Part Of: Neuroscience. Volume 434(2020)
• Page Start: 148
• Page End: 160
• Publication Date: 2020-05-10
• Subjects: BPA bisphenol-A -- GODT grating orientation discrimination test -- ip intraperitoneal -- LTP long-term potentiation -- OF Open field test -- PFC prefrontal cortex -- V1 primary visual cortex; bisphenol A -- visual discrimination -- orientation sensitivity -- signal-to-noise ratio -- IL-1β; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2020.03.035
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: BPA exposure during gestation and lactation decayed the orientation discrimination of rat pups. BPA exposure disturbed the response properties of visual neurons for orientation detection. BPA exposure caused the decrease of synaptic plasticity of pyramidal neurons in the primary visual cortex. IL-1β involves in the BPA-induced functional and structural impairment in the primary visual cortex. Abstract: Bisphenol-A (BPA) exposure can affect cognitive functions of rodents and humans. However, whether information inputs for these functions in the brain are perturbed by BPA remains unclear. Here, visual perception in rats was assessed by testing their ability to discriminate between vertical and horizontal grating. We found that BPA exposure (1 mg/kg/day) during gestation and lactation markedly decreased the grating discrimination ability in rat pups (postnatal 21 days). The results of neuronal functions in the primary visual cortex (V1) showed that the orientation selectivity and signal extraction ability and fidelity were notably decreased after BPA exposure. These effects were accompanied by a reduction in synaptic plasticity (i.e., spine density and maturity) in the V1. According to inflammatory factor expression and glial cell morphology, no increase in inflammatory activation was observed after BPA exposure. However, BPA-exposed rat pups exhibited a significant decrease in IL-1β expression in the V1, accompanied by a decline in P38 phosphorylation. After local injection of IL-1β (10 ng/ml) in the V1, these two visual properties recovered to normal levels. Thus, our findings imply that physiological dysfunction of IL-1β may contribute to orientation perception deficits in BPA-exposed rats.