EN
Mutations in several genes and gene copy number variants are associated with neurodevelopmental disorders including autism spectrum disorders (ASD). Several gene products putatively implicated in ASD are frequently part of signaling networks involved in synapse formation and/or function leading to changes in the balance between excitation and inhibition (E/I balance). The network of parvalbumin (PV)-expressing interneurons has gained particular attention in ASD, yet not much is currently known on PV’s possible role with respect to ASD. PV-knockout mice were subjected to a battery of behavioral experiments testing for ASDlike, schizophrenia-like and anxiety-related behavior. PV-/- mice display the three core symptoms present in ASD patients: impaired social interactions, reduced communication and repetitive and stereotyped behavior. In addition, they also show ASDassociated developmental neuroanatomical changes in the neocortex and the cerebellum. Using electrophysiology, we observed that the E/I balance is altered by modification of both, inhibitory and excitatory synaptic transmission. Based on the reported changes in PV expression pattern in numerous mouse ASD models, we suggest a convergent pathway in ASD, where mutations in ASDlinked genes may lead to (homeostatic) adaptations causing a down-regulation of PV that ultimately results in the ASD phenotype.