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Summary: This study shows that neuroligins are involved in autism spectrum disorder, and that dysfunction of NMDA receptors and PV+ interneurons in the medial prefrontal cortex contribute to social deficits in a mouse model of autism. The researchers found that restoring NMDA receptor function with a partial agonist improved the interneuron dysfunction and prevented social deficits. These findings suggest that targeting NMDA receptors and PV+ interneurons may be a potential therapeutic strategy for autism.
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Correction
Neurosciences
Wei Cao, Shen Lin, Qiang-qiang Xia, Yong-lan Du, Qian Yang, Meng-ying Zhang, Yi-qing Lu, Jing Xu, Shu-min Duan, Jun Xia, Guoping Feng, Junyu Xu, Jian-hong Luo
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Neurosciences
Qiang-qiang Xia, Prathibha Sekar, Craig M. Powell
Summary: This study suggests that environmental factors play a more significant role than genetics in modulating autism behavior, and the underlying neural circuit mechanisms are investigated in detail.
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Cell Biology
Wei Cao, Jia-hui Li, Shen Lin, Qiang-qiang Xia, Yong-lan Du, Qian Yang, Ying-zhi Ye, Ling-hui Zeng, Xiang-yao Li, Junyu Xu, Jian-hong Luo
Summary: This study shows that neuroligins are involved in autism spectrum disorder, and that dysfunction of NMDA receptors and PV+ interneurons in the medial prefrontal cortex contribute to social deficits in a mouse model of autism. The researchers found that restoring NMDA receptor function with a partial agonist improved the interneuron dysfunction and prevented social deficits. These findings suggest that targeting NMDA receptors and PV+ interneurons may be a potential therapeutic strategy for autism.
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Multidisciplinary Sciences
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Summary: Autism Spectrum Disorder (ASD) is a developmental disorder characterized by repetitive behavior, restricted range of interests, and atypical social interaction and communication. The CUL3 gene, which codes for a scaffold protein involved in assembly of ubiquitin ligase complexes, has been identified as a high-risk gene for autism. In a mouse model, heterozygous deletion of Cul3 leads to reduced CUL3 protein levels and impaired spatial object recognition memory, but does not cause major abnormalities in hippocampal neuronal morphology, function, or social interaction.