DIVIDING THE SOCIAL BRAIN: DIVERGENT GENETIC FUNCTIONS OF NONAPEPTIDES IN SOCIAL DECISION-MAKING

Social living in vertebrates is defined by the commonness of adaptive decisions, rather than developmentally fixed roles. Whether this relies on the emergence of dedicated mechanisms has implications for managing social needs, which are increasingly recognised as a catalyst for both mental and physical health. From social rank and tend-and-defend functions, to prosocial and antisocial controls and the social regulation of stress, the oxytocin and vasotocin/vasopressin signalling pathways arise as key candidates. The two nonapeptide mechanisms emerged in vertebrates from a single ancestral one following gene duplication events in fish. However, it is yet unclear if these genetic changes gave rise to a neurocognitive mechanism dedicated to social decisions. We addressed this in zebrafish, a present-day model of ancestral nonapeptide systems, by examining functional mutation deficits in groups, the genetic necessity and pharmacological rescue of sociocognitive functions, and the role of constitutive transcriptional changes in forebrain regions. Individually tracked in groups, oxytocin and vasotocin mutants had contrasting and differential deficits across kinematics, interaction rates, network metrics and collective responses, as well as on derivative behavioural clusters. In individual decision paradigms, oxytocin was necessary and sufficient for recognition-based biases and for aggressive approach, while vasotocin for affiliative approach and retreat in aggressive contexts. These genetically derived divergent functions suggest that nonapeptides evolved specialised roles across cognitive and motivational dimensions of social decisions. I will discuss how this adaptation is further supported by whole-transcriptome differential expression controls in the brain, giving insight on the role of nonapeptides across neural processes.