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Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder characterized by core symptoms of impaired social behavior and communication. Recent studies have suggested that the oxytocin system, which regulates social behavior in mammals, is potentially involved in ASD. Mouse models of ASD provide a useful system for understanding the associations between an impaired oxytocin system and social behavior deficits. However, limited studies have shown the involvement of the oxytocin system in the behavioral phenotypes in mouse models of ASD. We have previously demonstrated that a mouse model that carries the ASD patient-derived de novo mutation in the  pogo transposable element derived with zinc finger domain  ( POGZ  WT/Q1038R  mice), showed ASD-like social behavioral deficits. Here, we have explored whether oxytocin (OXT) administration improves impaired social behavior in  POGZ  WT/Q1038R  mice and found that intranasal oxytocin administration effectively restored the impaired social behavior in  POGZ  WT/Q1038R  mice. We also found that the expression level of the oxytocin receptor gene ( OXTR ) was low in  POGZ  WT/Q1038R  mice. However, we did not detect significant changes in the number of OXT-expressing neurons between the paraventricular nucleus of  POGZ  WT/Q1038R  mice and that of WT mice. A chromatin immunoprecipitation assay revealed that POGZ binds to the promoter region of  OXTR  and is involved in the transcriptional regulation of  OXTR . In summary, our study demonstrate that the pathogenic mutation in the  POGZ , a high-confidence ASD gene, impairs the oxytocin system and social behavior in mice, providing insights into the development of oxytocin-based therapeutics for ASD.   Supplementary Information  The online version contains supplementary material available at 10.1186/s13041-021-00769-8.

Intranasal oxytocin administration ameliorates social behavioral deficits in a POGZWT/Q1038R mouse model of autism spectrum disorder