| First Author | Yamamuro K | Year | 2020 |
| Journal | Nat Neurosci | Volume | 23 |
| Issue | 10 | Pages | 1240-1252 |
| PubMed ID | 32868932 | Mgi Jnum | J:359723 |
| Mgi Id | MGI:7788953 | Doi | 10.1038/s41593-020-0695-6 |
| Citation | Yamamuro K, et al. (2020) A prefrontal-paraventricular thalamus circuit requires juvenile social experience to regulate adult sociability in mice. Nat Neurosci 23(10):1240-1252 |
| abstractText | Juvenile social isolation reduces sociability in adulthood, but the underlying 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 neurons projecting to the posterior paraventricular thalamus (mPFC-->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 medial prefrontal cortex excitatory and inhibitory neuron populations required for sociability that are profoundly affected by juvenile social experience. |
