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C03: Distributed network control and interventions to frustrative non-reward and threat triggered aggressions

Investigate context-dependent aggression triggered by frustrative non-reward or acute social threats. Using newly developed approaches, multiple behavioral domains will be assessed in a semi-naturalistic, autonomous mouse habitat. Specifically, the habitat assesses the inter-individual dynamics of social interactions, aggressions, and hierarchy and the individual reward learning and impulsivity through different integrated modules. Intermittent challenges comprise intruder aggression and frustrative non-rewards. Within this LCD, circuit mechanisms are dissected through chemogenetic interventions, in vivo recordings, and functional MRI in awake mice during task performance. This approach in the first funding period will enable us to disentangle the specific functions of candidate entry points in prefrontal to ventral striatum pathways with respect to their modulation of aggression and dominance for potential interventions.

Contributors


Publications


Stable clique membership in male mouse societies requires oxytocin-enabled social sensory states

The ability to establish stable de novo relationships in complex environments is essential for social functioning but disrupted in disorders such as autism. Yet, the mechanisms supporting higher-order bonding in large groups remain unclear. Here, we introduce a naturalistic model of clique formation in mouse societies, using longitudinal tracking from large-scale video data. We show that small, stable cliques emerged from the specific group configurations. Consistently, also kinship did not significantly facilitate entry. These cohesive cliques resembled human mutually interacting rich-clubs, exhibiting high social rank and influence over non-members. We next examined whether oxytocin signaling in the olfactory cortex supports such higher-order bonding. Despite preserved social motivation, mice with conditional oxytocin receptor deletion in this sensory cortex failed to join rich-clubs, approached peers less consistently, and received unstable reciprocal connections. This network-level disorganization demonstrates how social dynamics can magnify individual deficits. Our findings identify oxytocin-dependent social sensory states as a necessary mechanism for forming stable relationships in complex social networks.