Effects of adolescent social isolation and resocialization on the mOFC-BLA synaptic transmission and social behavior in mice.

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Early-life social experience is critical for the development of social cognition, and early social deprivation induces alteration of sociality in animals and human. The medial orbitofrontal cortex (mOFC) to basolateral amygdala (BLA) pathway is one of the critical circuit for social behavior. Hence, the mOFC-BLA pathway may be functionally sensitive for early social environment, and its dysfunction may cause changes in social behaviors. Here, we examined effects of social isolation (SI) and resocialization (RS) on mOFC-BLA synaptic functions in mice. First, we isolated the mice during early (3-5 weeks of age) or late (6-8 weeks of age) adolescence and assessed sociality and mOFC-BLA synaptic properties using optogenetic and patch-clamp methods. SI in early-adolescent, but not late adolescent, decreased sociality and AMPA/NMDA current ratio in the mOFC-BLA synapse. Then, we examined the effects of RI during late adolescence or adulthood (9-11 weeks of age), on SI-induced synaptic and social deficit. RS in late adolescence, but not adulthood, recovered SI-induced social deficit and mOFC-BLA synaptic change. These results suggested that SI disrupted mOFC-BLA synaptic function in early adolescence and caused social deficit, and restorative effect of RS on SI-induced behavioral and synaptic change limited until late adolescence.