Altered sensory experience is now considered a key feature of neurodevelopmental and autism spectrum disorders (ASD). This alteration results in, and often predicts, a range of cognitive, social, and behavioural affective impairments, strongly impacting the quality of life. However, the underlying neurophysiological mechanisms that disrupt sensory perception remain understudied. We investigated these mechanisms in a mouse model of SYNGAP1 haploinsufficiency (ΗΕΤ), SYNGAP1 being one of the most prevalent neurodevelopmental disorder genes. Using in vivo two-photon calcium imaging, we found that layer 2/3 neurons in the primary visual cortex (V1) of Syngap HET mice responded to visual stimuli with greater variability compared to wild-type littermate controls, resulting in a reduction in V1 coding precision and reduced behavioural visual discriminability. This impairment was not due to altered intrinsic and synaptic properties of V1 HET neurons. Notably, when we tested V1 visual responses under anaesthesia, we found that the variability of visual responses and population coding precision in V1 neurons of Syngap HET mice were restored to control levels. These results indicate that anaesthesia-dependent inputs are responsible for the visual impairments found in Syngap HET mice and suggest a dysregulation of behavioural state modulation. Top-down, neuromodulatory inputs may therefore be promising therapeutic targets for improving sensory experience of individuals with SYNGAP1 haploinsufficiency and more generally, other neurodevelopmental disorders.