Secondary organic aerosol (SOA) is a major component of PM 2.5 and formed in the atmosphere by oxidation of products from anthropogenic and biogenic volatile organic compounds. Recently, we have shown that the single intranasal instillation of diesel exhaust origin secondary organic aerosol (DE-SOA) increased expression of proinflammatory cytokines and their signal transduction pathway genes in lung of BALB/c mice. In the present study, we aimed to investigate the effects of inhalation exposure to DE-SOA on learning and maternal behavior in mice. We generated the SOA by oxidation of diesel exhaust particle (DEP) mixed with ozone. Male BALB/c mice were exposed clean air (control), diesel exhaust (DE), DE-SOA and filtered DE (gas only) in the inhalation chambers for one or three months (6 h/day, 5 days/week) and examined learning ability by a novel object recognition test and memory function-related gene expressions in the hippocampus by a real-time RT-PCR method. Moreover, female mice exposed to DE-SOA for one month before mating were examined maternal behaviors and their related gene expressions in the hypothalamus. Decreased novel object recognition ability and up-regulation of N-methyl-D aspartate (NMDA) receptor expression were observed in both of one or three month DE-SOA-exposed male mice. Furthermore, decreased maternal behavior and the expression level of estrogen receptor (ER)-alpha, and oxytocin receptor were found in DE-SOA-exposed dam compared with the control. Among the constituents of DE-SOA, organic carbon is the potential candidate to induce neurotoxicity. Our present study suggests that the exposure to DE-SOA may induce neurotoxicity and affect learning and maternal behavior by modulating the gene expressions in the hippocampus and hypothalamus of mice.