Atypical sensory processing affects approximately 90% of individuals with autism spectrum disorder (ASD) and has been recently considered a core ASD symptom. In accordance with neurophysiological findings in human subjects, preclinical studies have found altered activity of primary sensory neocortices and sensory association areas following sensory stimuli and perceptual paradigms in several genetic mouse models of ASD. Attention deficits are a common comorbidity of autism and may impact other symptoms. Indeed, recent research suggests that alterations in attention and sensory processing are interrelated in ASD, and that attention might be a significant predictor of how sensory information is perceived and integrated, and that both significantly impact social engagement, communication and learning. Cognitive function requires the appropriate pre-attentive filtering of sensory information, a process that, in addition to sensory cortices, also involves the prefrontal cortex due to its role in bottom-up and top-down control of attention and sensory information processing. We therefore asked whether prefrontal cortex (PFC) function is altered in a well-established genetic mouse model of atypical sensory experience in autism. To test this, we used two behavioral tasks (in which the PFC has been implicated), combined with miniscope calcium imaging in freely moving Fmr1KO mice. Preliminary results from our team demonstrates that PFC function is altered in this model, as well as the input map of PFC neurons engaged in one of these tasks. Our current work extends these findings, pointing to behavioral and neurophysiological markers for exploring the attentional modulation of sensory information in Fmr1KO mice.