Prenatal exposure to particulate matter impairs offspring behavior via hippocampal NMDA receptor reduction: an in vivo and ex vivo study

Authors: Yunkyung Eom, Hye Kyung Lee, Yeong-Kyeong Kim, Seonwoo Yang, Yong-Hyeon Yim, Soyoung Shin, Jung-Woong Kim, Hee Min Yoo, and Sung Hoon Lee

Environment International, 20 April 2026

Maestro MEA recordings reveal how particulate matter exposure disrupts neuronal network activity and NMDA receptor signaling in a developmental neurotoxicity model. 

Air pollution and particulate matter exposure have been increasingly linked to adverse neurological outcomes, particularly during early brain development. However, the cellular and functional mechanisms underlying particulate matter–induced neurotoxicity remain poorly understood. In this study, researchers investigated how particulate matter exposure impacts neuronal network activity and NMDA receptor signaling in developing hippocampal neurons, with a focus on the neurotoxic effects of polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (BaP). 

Using Axion Biosystems’ Maestro MEA platform, the team performed electrophysiological recordings to evaluate how particulate matter exposure altered neuronal network function. The researchers observed that particulate matter exposure reduced network burst rate while increasing spikes per network burst, indicating disrupted network organization and altered excitability. These functional changes suggested impaired synaptic signaling and reduced coordination across developing neuronal networks. 

To further investigate the mechanism underlying this phenotype, the researchers examined NMDA receptor involvement by exposing cultures to NMDA in combination with benzo[a]pyrene. Their findings suggest that prenatal particulate matter exposure suppresses NMDA receptor function, potentially through PAH-mediated mechanisms, leading to reduced neuronal activity and impaired hippocampal network function. 

Together, this work highlights the value of functional electrophysiology for studying developmental neurotoxicity and demonstrates how MEA-based assays can help uncover mechanisms linking environmental exposures to disrupted neuronal network development.