Effects of Early Bisphenol A Exposure on Cortical Excitatory and Inhibitory Balance and Behaviour in Mice

Lily Tran; Lynn Lukose

doi:10.18192/osurj.v5i2.7935

Effects of Early Bisphenol A Exposure on Cortical Excitatory and Inhibitory Balance and Behaviour in Mice

Authors

Lily Tran St. Mother Teresa High School, Ottawa, ON, Canada
Lynn Lukose St. Mother Teresa High School, Ottawa, ON, Canada

DOI:

https://doi.org/10.18192/osurj.v5i2.7935

Abstract

Exposure to endocrine-disrupting chemicals such as 4-[2-(4-hydroxyphenyl)propan-2-yl]phenol (BPA) during development has been linked to altered neurodevelopment and increased risk for autism spectrum disorder (ASD) (1-5). During pregnancy, BPA exposure occurs through ingestion of contaminated food or beverages from polycarbonate plastics and epoxy resin-lined containers, allowing it to enter maternal circulation and cross the placenta (6-7). A proposed neurobiological mechanism underlying ASD involves disruption of cortical excitatory/inhibitory (E/I) synaptic balance, critical for neural network function and behavioural regulation (3, 8-12). However, it remains unclear whether combined prenatal and early postnatal BPA exposure alters cortical E/I organization in a dose-dependent and sex-specific manner. This study will investigate how early-life BPA exposure influences cortical synaptic markers and ASD-relevant behaviours in C57BL/6J mice. Eighteen pregnant dams (n = 6 per group) will be randomly assigned to control (water), low-dose BPA, or high-dose BPA groups. Through oral gavage, BPA will be administered from gestational day 0 through postnatal day 21 (PND21), targeting a critical window of synaptogenesis. This study will include only full-term offspring. BPA doses will model environmentally relevant human exposure (13-15). The experiment will divide offspring into molecular and behavioural cohorts. Molecular analyses will quantify excitatory (VGLUT1, PSD-95) and inhibitory (GAD67) synaptic markers using immunohistochemistry and western blotting to calculate cortical E/I ratios at PND21. Adolescent offspring will undergo behavioural testing between PND35 and PND60, including the three-chamber social interaction and open-field tests to assess sociability and anxiety-related behaviours. The study expects to determine that early-life BPA exposure produces dose-dependent and sex-specific alterations in cortical E/I balance accompanied by ASD-relevant behavioural changes (1, 3, 16-21). By integrating molecular and behavioural outcomes, this study will clarify whether early-life BPA exposure disrupts cortical E/I balance, a neurobiological feature implicated in ASD. This link would strengthen mechanistic evidence that environmental chemicals influence neurodevelopment and guide public health strategies to reduce exposure during critical developmental periods

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Published

2026-06-17

Issue

Vol. 5 No. 2 (2026)

Section

Ottawa Science Innovation Challenge Abstracts

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