Accumulating evidence implicates environmental particulate matter (PM) exposure as a risk factor for neurodevelopmental disorders. Because the developing brain is highly vulnerable to environmental toxicants, prenatal PM exposure may cause disproportionate toxicity in offspring. However, the neuronal mechanisms underlying PM-induced neurotoxicity remain unclear. Here, we investigated the effects of prenatal PM exposure on offspring behavior and hippocampal neuronal function. Prenatal intranasal administration of urban PM (200 and 400 μg/kg) induced cognitive deficits, hyperactivity, and anxiety-like behaviors. Notably, 200 μg/kg PM caused neurobehavioral abnormalities without affecting development or lung function. Transcriptomic analysis revealed altered hippocampal genes associated with neuronal development and synaptic organization. PM exposure reduced hippocampal N-methyl-D-aspartate (NMDA) receptor expression and disrupted spontaneous neuronal activity and synaptic networks in ex vivo hippocampal neurons. In contrast, glial inflammatory responses were unchanged, suggesting neuronal vulnerability as a primary target. Benzo[a]pyrene (BaP), a toxic PM constituent, reproduced these neuronal effects. Importantly, NMDA application restored aberrant neuronal activity in PM- and BaP-exposed neurons. These findings demonstrate that prenatal PM exposure impairs offspring neurobehavior through neuronal NMDA receptor dysfunction, even without developmental or pulmonary toxicity.