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Bisphenol-A Exposure during Gestation and Lactation Causes Visual Perception Deficits in Rat Pups Following a
Fan Hu1, Linke Zhang1, Tingting Li1
1School of Food and Biological Engineering, Hefei University of Technology, Hefei, Anhui 230009, People's Republic of China.
Insights
Bisphenol-A (BPA) exposure impairs visual perception and neuronal function in rat pups. This study suggests that reduced Interleukin-1 beta (IL-1β) levels in the brain contribute to these BPA-induced visual deficits.
Area of Science:
- Neuroscience
- Toxicology
- Developmental Biology
Background:
- Bisphenol-A (BPA) is a common environmental contaminant linked to cognitive impairments.
- The specific impact of BPA on sensory information processing, particularly visual input, remains incompletely understood.
Purpose of the Study:
- To investigate the effects of gestational and lactational BPA exposure on visual perception and neuronal function in the primary visual cortex (V1) of rat pups.
- To elucidate the underlying mechanisms, focusing on synaptic plasticity and inflammatory pathways.
Main Methods:
- Assessment of grating discrimination ability in rat pups exposed to BPA (1 mg/kg/day).
- Electrophysiological recordings and analysis of synaptic plasticity markers (spine density and maturity) in the V1.
- Measurement of inflammatory factors (IL-1β) and signaling pathways (P38 phosphorylation) in the V1.
- Intervention with IL-1β to assess recovery of visual function.
Main Results:
- BPA exposure significantly reduced grating discrimination ability in rat pups.
- Neuronal function in the V1 showed decreased orientation selectivity, signal extraction, and fidelity.
- Synaptic plasticity in the V1 was impaired, evidenced by reduced spine density and maturity.
- BPA exposure led to decreased IL-1β expression and P38 phosphorylation in the V1 without signs of general inflammation.
- Local administration of IL-1β restored visual properties in BPA-exposed rats.
Conclusions:
- Gestational and lactational BPA exposure negatively impacts visual perception and V1 neuronal function in developing rats.
- Reduced IL-1β signaling in the V1 is a key mechanism contributing to BPA-induced visual processing deficits.
- Targeting IL-1β pathways may offer therapeutic potential for mitigating BPA's neurodevelopmental effects.
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.
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