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Teratogenicity

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Related Experiment Video

Updated: Dec 25, 2025

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

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.

|March 31, 2020

Summary

This summary is machine-generated.

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.

Keywords:

IL-1β bisphenol A orientation sensitivity signal-to-noise ratio visual discrimination

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Published on: April 26, 2018

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.