Bidirectional Control of Infant Social Behavior by Dopaminergic Innervation of the Basolateral Amygdala

Social interaction deficits seen in psychiatric disorders emerge in early-life and are most closely linked to aberrant neural circuit organization and function. Due to technical limitations, we have had little understanding of the typical ontogeny of social behavior neural circuits or how early caregiving adversity impacts infant neurobiology to perturb lifelong social interaction. Using a suite of invasive procedures in awake, behaving young infant rats, including optogenetics, microdialysis and microinfusions, we charted the gradual increase in social behavior deficits following adversity-rearing and dissected circuits controlling this process. Persistently elevated dopamine in basolateral amygdala (BLA) was necessary and sufficient in initiating social behavior pathology, as demonstrated by manipulation of amygdala dopamine during adversity and during expression of social behavior deficits with the mother and peers.  Taken together, these data highlight mesolimbic dopamine circuit organization and function as a potential therapeutic target in understanding behavioral deficits associated with psychiatric disorders.