Top Highlights

• Chemogenetic stimulation of OT neurons at the neonatal stage ameliorated social deficits in early adulthood, concurrent with a cell-type-specific sustained recovery of the pivotal gene expressions within parvocellular OT neurons.
• The applicability of this framework to neurodevelopmental disorders remains uncertain, particularly those characterized by atypical social behaviors such as autism spectrum disorder.
• A recent seminal study employing single-cell RNA sequencing (RNA-seq) has unveiled distinct transcriptomic signatures of magnocellular and parvocellular PVHOT neurons, with the latter displaying an enriched expression of ASD risk factor genes21 and playing a more significant role in social reward12.
• To examine the generality of these findings, we conducted similar experiments in mice born to mothers that had been fed a high-fat diet, which we refer to as the maternal high-fat diet (MHFD) group for simplicity (Fig. 1h).
• These results indicate that two independent mouse models exhibiting atypical sociability due to exogenous or maternal factors commonly display reduced OT ligand expression in parvocellular PVHOT neurons.

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