Speaker
Description
The ability to form stable de novo relationships in complex environments is essential for social functioning and is impaired in severe psychiatric disorders including autism. Yet, the neurobiological basis and cognitive processes enabling the formation of stable bonds in larger groups remain poorly understood, thereby limiting our ability to develop effective therapies. Here, we establish a semi-naturalistic model of clique formation in mouse societies, where individuals are tracked longitudinally from massive video data. Small, stable rich-clubs develop within these mouse social networks. Consistent with human rich-clubs, these cohesive cliques tend to have high social rank and exert influence on non-members. Interestingly, neither prior rich-club-membership in a different group nor kinship facilitate entry into rich-clubs. Mimicking sparse population genetics, we probed the open question whether a subtle neuro-cognitive phenotype, namely impaired induction of social sensory processing states by cortical oxytocin signaling, impair higher-order social bonding in these complex social environments. Despite preserved social motivation, mice with alterations in this oxytocin subsystem fail to join rich clubs. They approached group members less consistently, and connections from others towards them fluctuated more as well. This reciprocal disorganization highlights how interactional dynamics within social networks can amplify individual-level deficits, consistent with models of emergent properties of social behavior. These findings underscore the role of oxytocin in tuning sensory systems into a social processing state, with profound implications for an individual's ability to establish stable relationships in complex social networks.
