Effets de l’exposition précoce au bisphénol A sur l’équilibre et le comportement excitateurs et inhibiteurs corticales chez la souris

Auteurs-es

  • 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

Résumé

L’exposition à des substances perturbatrices endocriniennes telles que le 4-[2-(4-hydroxyphényl)propane-2-yl]phénol (BPA) au cours du développement a été associée à un neurodéveloppement altéré et à un risque accru de trouble du spectre de l’autisme (TSA) (1-5). Pendant la grossesse, l’exposition au BPA se produit par l’ingestion d’aliments ou de boissons contaminés provenant de plastiques polycarbonates et de contenants doublés de résine époxy, ce qui lui permet d’entrer dans la circulation maternelle et de traverser le placenta (6-7). Un mécanisme neurobiologique proposé sous-jacent au TSA implique la perturbation de l’équilibre synaptique cortical-excitateur/inhibiteur (E/I), essentiel au fonctionnement des réseaux neuronaux et à la régulation comportementale (3, 8-12). Cependant, il reste incertain si l’exposition combinée prénatale et précoce au BPA postnatal modifie l’organisation corticale de l’E/I de manière dépendant de la dose et spécifique au sexe. Cette étude étudiera comment l’exposition au BPA au début de la vie influence les marqueurs synaptiques corticales et les comportements liés au TSA chez les souris C57BL/6J. Dix-huit mères gestantes (n = 6 par groupe) seront assignées au hasard aux groupes témoins (eau), à faible dose de BPA ou à forte dose de BPA. Par voie orale, le BPA sera administré du jour 0 gestationnel au jour postnatal 21 (PND21), ciblant une fenêtre critique de synaptogenèse. Cette étude n’inclura que les enfants à terme. Les doses de BPA modélisent l’exposition humaine environnementale (13-15). L’expérience divisera la descendance en cohortes moléculaires et comportementales. Les analyses moléculaires quantifieront les marqueurs synaptiques excitateurs (VGLUT1, PSD-95) et inhibiteurs (GAD67) en utilisant l’immunohistochimie et le transfert de protéines pour calculer les rapports corticaux E/I à PND21. Les enfants adolescents subiront des tests comportementaux entre PND35 et PND60, incluant les tests d’interaction sociale à trois chambres et des tests en champ ouvert pour évaluer la sociabilité et les comportements liés à l’anxiété. L’étude s’attend à déterminer que l’exposition au BPA au début de la vie entraîne des altérations dépendantes de la dose et spécifiques au sexe dans l’équilibre cortical/E/I, accompagnées de changements comportementaux liés au TSA (1, 3, 16-21). En intégrant les résultats moléculaires et comportementaux, cette étude clarifiera si l’exposition au BPA au début de la vie perturbe l’équilibre cortical/E/I, une caractéristique neurobiologique impliquée dans le TSA. Ce lien renforcerait les preuves mécanistes que les substances chimiques environnementales influencent le neurodéveloppement et guiderait les stratégies de santé publique pour réduire l’exposition durant les périodes critiques du développement.

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Publié-e

2026-06-17

Numéro

Vol. 5 No. 2 (2026)

Rubrique

Ottawa Science Innovation Challenge Abstracts

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