Autism spectrum disorders (ASD) is a developmental disorder with an estimated prevalence of _~1.6%. Growing financial and caregiving burdens for patients’ families are getting social problems. Diagnostic criteria of ASD include deficits in social communications and interactions, restricted interests, and repetitive behaviors. Based on studies of monozygotic and dizygotic twins, it has been proposed that a part of ASD is a genetic disorder. Indeed, many causative genes of ASD, such as Autism susceptibility candidate 2 (AUTS2) have been identified. It has been reported that the murine orthologue of AUTS2, Auts2 activates a small GTPase Rac1, and thus regulates neuronal migration by forming lamellipodia at the growth cone. Given that lamellipodia play crucial roles in synapse formation as well, we estimated synapse numbers in Auts2 mutant mouse in this study. Excitatory synapses were immunolabeled by antibodies to Bassoon and Homer1, markers for pre-synapse and excitatory post-synapse respectively. Synapses at hippocampal CA1 region were imaged with super-resolved three-dimensional stimulated emission depletion (3D-STED) microscopy. As a result, we discovered the change of the number of excitatory synapses in Auts2 mutant mouse. Our finding sheds light on unidentified pathological changes in ASD at the synapse level.