A. S. J. Nicolson

Social organization and division of labour are fundamental to animal societies^1,2,3, yet how these structures emerge from individual interactions and are shaped by neuromodulation remains unclear. Here, using behavioural tracking in a semi-natural environment, neural recordings and computational models that integrate reinforcement learning and social condition, we show that triads of isogenic mice develop specialized roles spontaneously while solving a foraging task under social constraints. Notably, despite minor intra-sex differences in behaviour when mice were tested alone, male triads formed stable worker–scrounger relationships driven by competition, whereas female triads adopted uniform, cooperative strategies. These sex-divergent roles were shaped by dopaminergic activity in the ventral tegmental area. Model analysis revealed how intra-sex and inter-sex parameter differences in resource exploitation, combined with contingent social interactions, drive behavioural specialization and division of labour. Most notably, it highlighted how contingency, amplified by competition, magnifies individual differences and shapes social profiles. The plastic, adaptive nature of social organization was apparent when sex mixing or reintroducing experienced individuals into naive groups reshaped role distribution. Furthermore, dopaminergic manipulations confirmed this plasticity, reshaping roles and altering group structure. Our findings support a multi-scale feedback loop whereby social context shapes neural states, which in turn reinforce behavioural specialization and stabilize social structures.

Stress can drive overconsumption of high-fat foods. The medial prefrontal cortex (mPFC) is implicated in such stress-eating, but the underlying circuit mechanisms remain unclear. Here, we show that mPFC projections to the lateral hypothalamus (LHA) are required for stress-induced fat intake in male mice. We find that mPFC-LHA stimulation in sated states increases fat intake. Social stress acutely engages mPFC-LHA neurons, and inhibiting this pathway selectively prevents stress-driven excess fat intake. Circuit mapping shows that mPFC neurons innervate GABAergic and glutamatergic LHA (LHA _VGLUT2 ) neurons, but that social stress preferentially engages mPFC-LHA _VGLUT2 neurons and causes plasticity at mPFC-LHA _VGLUT2 synapses. Specifically, stress weakens mPFC synapses onto LHA _VGLUT2 neurons that curtail food intake, while strengthening mPFC synapses onto midbrain-projecting LHA _VGLUT2 neurons linked to stress-eating. We show that LHA _VGLUT2 neurons are required downstream mPFC targets for transforming stress into heightened fat intake. Overall, we identify the mPFC-LHA as a multi-branched network, indispensable for stress-eating.