Social Communication Deficits in Synapsin II Knockout Mice

Autism spectrum disorders (ASD) are heterogeneous neurodevelopmental disorders characterized by deficits in social interaction and social communication, restricted interests and repetitive behaviors. Abnormalities in language development, mental retardation and epilepsy are often observed in autistic children and, conversely, several forms of epilepsy also display ASD. Given the high comorbidity between ASD and epilepsy, the possibility of a common genetic basis for both diseases has been proposed. Synapsins (Syns) are a family of synaptic vesicle phosphoproteins encoded by the SynI, SynII and SynIII genes. The Syn gene family is a good candidate for the synaptic epilepsy/ASD pathway, as Syns regulate synaptic transmission and plasticity with distinct roles in excitatory and inhibitory neurons. Aim of our study was to analyze whether deletion of SynII gene in mice causes social communication deficits. Analysis of social and vocal repertoires revealed a clear social investigation defi