Juvenile social isolation reduces sociability in adulthood, but the neural circuit mechanisms are poorly understood. We found that, in male mice, 2 weeks of social isolation immediately following weaning leads to a failure to activate medial prefrontal cortex (mPFC) neurons projecting to the posterior paraventricular thalamus (pPVT) during social exposure in adulthood. Chemogenetic or optogenetic suppression of mPFC->pPVT activity in adulthood was sufficient to induce sociability deficits without affecting anxiety-related behaviors or preference toward rewarding food. Juvenile isolation led to both reduced excitability of mPFC->pPVT neurons and increased inhibitory input drive from low-threshold spiking somatostatin interneurons in adulthood, suggesting a circuit mechanism underlying sociability deficits. Chemogenetic or optogenetic stimulation of mPFC->pPVT neurons in adulthood could rescue the sociability deficits caused by juvenile isolation. Our study identifies a pair of specific mPFC excitatory and inhibitory neuron populations required for sociability that are profoundly affected by juvenile social experience.
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