Perception, a cognitive construct, emerges through sensorimotor integration (SMI). The molecular and cellular mechanisms that shape SMI within circuits that promote cognition are poorly understood. Here, we demonstrate that expression of the autism/intellectual disability gene, Syngap1, in mouse cortical excitatory neurons promotes touch sensitivity required to elicit perceptual behaviors. Cortical Syngap1 expression enabled touch-induced feedback signals within sensorimotor loops by assembling circuits that support tactile sensitivity. These circuits also encoded correlates of attention that promoted self-generated whisker movements underlying purposeful and sustained object exploration. As Syngap1 deficient animals explored objects with whiskers, relatively weak touch signals were integrated with relatively strong motor signals. This produced a signal-to-noise deficit consistent with impaired tactile sensitivity, reduced tactile exploration, and weak tactile learning. Thus, Syngap1 expression in cortex promotes tactile perception by assembling circuits that integrate touch and whisker motor signals. Deficient Syngap1 expression likely contributes to cognitive impairment through abnormal top-down SMI.