In utero exposure to NMDA receptor autoantibodies disrupts hippocampal circuit maturation

Résumé fourni par la source

imaging and computational modeling reveal that this deficit compromises early synchronized network activity in neonatal CA1. In vivo, NR1 ABs hinder the emergence of continuous activity around eye opening-a critical milestone for later cognitive function-by reducing the ability of CA1 PCs to developmentally decouple from local network dynamics. Our findings implicate NR1 ABs as drivers of a developing hippocampal circuitopathy and highlight disrupted activity-dependent circuit refinement as a mechanistic link between maternal autoimmunity and neurodevelopmental dysfunction.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.