Fig. 1.

A working conceptual model of effects of ELS on amygdalostriatal interactions. Based on a synthesis of human and non-human animal research we suggest that ELS acts on neural systems associated with affective valuation by modulating (i.e., decreasing) the ability of the amygdala to send value-based information to the ventral striatum via unidirectional excitatory glutamatergic projections (denoted by dashed lines). During sensitive periods of development, ELS causes increases in the release and circulation of stress hormones (i.e., corticosterone, cortisol), which act not just to accelerate amygdala development but to interact with midbrain dopaminergic systems, resulting in the increased release of dopamine into the amygdala and the ventral striatum. The increased levels of dopamine may be inappropriately regulated as a function of ELS, leading to subsequent neural and behavioral phenotypes associated with the emergence of behaviors during adolescence associated with internalizing illness such as anxiety and depression that may persist into adulthood.