Section For many species, access to crucial resources, such as food, protection, and receptive mates, requires a highly coordinated and adaptable system of social behavior. Although the sensitivity of social behavior to previous experience can be adaptive, it also can be detrimental: research has shown that early-life experience, particularly trauma associated with a caregiver, has a unique ability to program social deficits that last well into adulthood. Data from a variety of species appears to converge on the amygdala as a central mediator of these impairments in social behavior. However, the specific role of the amygdala in producing social deficits following abuse, or whether this changes over the course of development, remain unclear. To address this gap in knowledge, and with an eye toward developing interventions, we propose to study social behavior and functional amygdala circuitry in a rodent model of early life abuse. Data from our lab and pilot data collected for this proposal supports the hypothesis that caregiver abuse produces persistent social deficits that emerge at weaning associated with dysregulation of amygdala circuitry, and that a period of environmental enrichment following abuse can prevent the emergence of impairments. Furthermore, the literature suggests a specific role for the basolateral (BLA) and central (CeA) amygdala nuclei in modulating social behavior. To test this, we have measured amygdala activation in rats that were reared in either typical (control) or abusive conditions during tests of social behavior at weaning and adulthood. Next, we will explore the efficacy of environmental enrichment on reversing the effects of early life abuse. Finally, we will dissect the amygdala circuitry causally involved in these effects using optogenetic tools. We have collected data showing that following abuse from a caregiver, peer social behavior deficits will emerge by weaning (PN23), persist into adulthood (PN60) and are linked to changes in BLA function. We hypothesize that 1) enrichment after abuse, but before emergence of neurobehavioral deficits induced by early-life abuse will restore typical social behavior and amygdala function, and 2) targeted optogenetic inhibition of the BLA-CeA circuit will normalize social behavior in abused animals to control levels. The work proposed here will begin to address the causal role of amygdala circuitry in producing social deficits following abuse and identify interventions to prevent emergence of neurobehavioral deficits following trauma.
Childhood abuse has been linked to lasting deficits in social behavior associated with changes in amygdala function, although the specific mechanisms that underlie these effects are unclear. The proposed studies are aimed towards identifying the mechanisms and neural circuitry underlying the enduring consequences for social behavior in a model of early-life abuse and to test an intervention to reduce those adverse effects.
