In the brain, peripheral immune cells are localized in specific regions such as meningeal space, choroid plexus, and perivascular spaces, and contribute to brain development. Previous cohort studies have shown that meningeal inflammation during neonatal periods is a potent risk factor for neurodevelopmental disorders such as attention-deficit hyperactivity disorders (ADHD), however, the pathological mechanism underlying neonatal meningeal inflammation-induced neurodevelopmental disorders has been still unclear. To elucidate the pathological mechanism of neurodevelopmental disorders caused by neonatal meningeal inflammation, we induced meningeal inflammation in neonatal mice, and found that neonatal meningeal inflammation-induced mice exhibited ADHD-like behaviors in adulthood. Histological analysis and adeno-associated virus-based neurotracing or pharmacogenetics showed increased dopaminergic inputs in the nucleus accumbens (NAc) was responsible for ADHD-like behaviors. Moreover, a large number of inflammatory macrophages was observed in the brain after inducing meningeal inflammation, and macrophage depletion inhibited ADHD-like behaviors. These results demonstrated that ADHD-like behaviors after neonatal meningeal inflammation is caused by the formation of aberrant dopaminergic synapses in NAc by inflammatory macrophages.