Increasing evidence suggests that ultrafine particle (UFP) air pollution may produce sustained brain inflammation. UFP might be predicted to produce brain effects similar to those seen with maternal/neonatal inflammation, components of which are considered models of schizophrenia, autism, cerebral palsy, mental retardation, and Parkinson's disease. Consistent with this possibility, preliminary data shows that postnatal UFP exposures results in sustained brain inflammation in mice as adults in ventral midbrain and hippocampus, brain regions key to mediating complex cognition and motor functions. Such residual inflammation suggests that developmental UFP exposure may represent a heretofore largely underappreciated risk factor for neurodevelopment dysfunction in children or a fetal risk factor for neurodegenerative diseases. In this study, researchers will test whether developmental UFP exposures of mice can affect cognitive and/or locomotor behavior. They will also explore cellular and molecular changes, including alterations in levels of brain cytokines, inflammation, oxidative stress, neurotransmitters and/or plasma corticosterone. Positive findings would suggest that UFP represents a previously underappreciated basis for brain dysfunction and could lead to significant advances in understanding the contribution of air pollutants to the etiology of neurodevelopment and neurodegenerative disorders, including autism.