Early life stress (ELS), in the form of childhood maltreatment, abuse, or neglect, increases the risk for psychiatric sequelae later in life. The neurobiology of response to early stress and of reward processing overlap substantially, leading to the prediction that reward processing may be a primary mediator of the effects of early life stress. We describe a growing body of literature investigating the effects of early life stressors on reward processing in animals and humans. Despite variation in the reviewed studies, an emerging pattern of results indicates that ELS results in deficits of ventral striatum-related functions of reward responsiveness and approach motivation, especially when the stressor is experienced in early in development. For stressors experienced later in the juvenile period and adolescence, the animal literature suggests an opposite effect, in which ELS results in increased hedonic drive. Future research in this area will help elucidate the transdiagnostic impact of early life stress, and therefore potentially identify and intervene with at-risk youth, prior to the emergence of clinical psychopathology.

Rationale Adverse social experience in adolescence causes reduced medial prefrontal cortex (mPFC) dopamine (DA) and associated behavioral deficits in early adulthood. Objective To determine whether mPFC DA hypofunction following social stress is specific to adolescent experience, and if this results from stress-induced DA D2 receptor activation. Materials and Methods Male rats exposed to repeated social defeat during adolescence or adulthood had mPFC DA activity sampled 17 days later. Separate experiments used freely-moving microdialysis to measure mPFC DA release in response to adolescent defeat exposure. At P40, 49 and 56 mPFC DA turnover was assessed to identify when DA activity decreased in relation to the adolescent defeat experience. Finally, non-defeated adolescent rats received repeated intra-mPFC infusions of the D2 receptor agonist quinpirole, while another adolescent group received intra-mPFC infusions of the D2 antagonist amisulpride before defeat exposure. Results Long-term decreases or increases in mPFC DA turnover were observed following adolescent or adult defeat, respectively. Adolescent defeat exposure elicits sustained increases in mPFC DA release, and DA turnover remains elevated beyond the stress experience before declining to levels below normal at P56. Activation of mPFC D2 receptors in non-defeated adolescents decreases DA activity in a similar manner to that caused by adolescent defeat, while defeat-induced reductions in mPFC DA activity are prevented by D2 receptor blockade. Conclusions Both the developing and mature PFC DA systems are vulnerable to social stress, but only adolescent defeat causes DA hypofunction. This appears to result in part from stress-induced activation of mPFC D2 autoreceptors.

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