The placental-mammal specific miR379-410 microRNA cluster restricts sociability in mice

Synaptic dysfunction is thought to underlie altered sociability in autism. However, the gene regulatory mechanisms that control synaptic protein expression in the context of social behaviour are poorly explored. Here we show that deletion of the large placental mammal specific miR379-410 cluster in mice leads to hypersocial behaviour, increased excitatory synaptic transmission and exaggerated expression of ionotropic glutamate receptor complexes in the hippocampus. Thus, interfering with miR379-410 could represent a novel therapeutic strategy for social deficits in autism.

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