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Abstract:
Social encounters are associated with varying degrees of emotional
arousal and stress. The mechanisms underlying adequate socioemotional
balance are unknown. The medial amygdala (MeA) is a brain region
associated with social behavior in mice. Corticotropin-releasing factor
receptor type-2 (CRF-R2) and its specific ligand urocortin-3 (Ucn3),
known components of the behavioral stress response system, are highly
expressed in the MeA. Here we show that mice deficient in CRF-R2 or Ucn3
exhibit abnormally low preference for novel conspecifics. MeA-specific
knockdown of Crfr2 (Crhr2) in adulthood recapitulated this phenotype. In
contrast, pharmacological activation of MeA CRF-R2 or optogenetic
activation of MeA Ucn3 neurons increased preference for novel mice.
Furthermore, chemogenetic inhibition of MeA Ucn3 neurons elicited
pro-social behavior in freely behaving groups of mice without affecting
their hierarchal structure. These findings collectively suggest that the
MeA Ucn3 CRF-R2 system modulates the ability of mice to cope with social
challenges.
