Exposure to air pollution, and particularly to particulate matter (PM), has been associated with higher rates of Multiple Sclerosis (MS) relapses and increased neuroinflammation in MS patients, suggesting that PM exposure may contribute to MS exacerbation. To address this issue, we have combined the induction of MOG35-55-induced experimental autoimmune encephalomyelitis (EAE) in mice – the most used animal model of MS - with PM10 exposure. Mice were exposed to PM10 dosages relevant for human exposure before the immunization or during the pre-symptomatic phase. In both cases, PM10 exposures did not significantly modify the disease course or the neuropathology of EAE mice. Yet, few hours after exposure, EAE mice exposed to PM10 during the pre-symptomatic phase (PM-EAE) showed specific behavioral alterations that couldn’t be observed neither in control EAE nor in PM-exposed wild-type mice. Namely, when tested in the Open Field, Elevated Plus Maze and Novel Object Recognition tests, PM-EAE mice showed risk-taking, impulsive behavior and a significant increase in novelty seeking. Since the observed behavioral phenotypes are frequently associated with alterations of the dopaminergic neurotransmission, along with neuroinflammation markers, we are now studying whether PM10 exposure in EAE mice is associated with changes in brain dopamine levels or in the expression of genes coding for dopamine receptors/transporters and their dynamics/recycling. Overall, while PM10 exposure did not alter the EAE course, it selectively induced behavioral changes in EAE mice, possibly interacting with their altered neuroimmune/neurotransmission background.