Stress-related anhedonia is associated with ventral striatum reactivity to reward and transdiagnostic psychiatric symptomatology

Abstract

Background Early life stress (ELS) is consistently associated with increased risk for subsequent psychopathology. Individual differences in neural response to reward may confer vulnerability to stress-related psychopathology. Using data from the ongoing Duke Neurogenetics Study, the present study examined whether reward-related ventral striatum (VS) reactivity moderates the relationship between retrospectively reported ELS and anhedonic symptomatology. We further assessed whether individual differences in reward-related VS reactivity were associated with other depressive symptoms and problematic alcohol use via stress-related anhedonic symptoms and substance use-associated coping. Method Blood oxygen level-dependent functional magnetic resonance imaging (fMRI) was collected while participants (n = 906) completed a card-guessing task, which robustly elicits VS reactivity. ELS, anhedonic symptoms, other depressive symptoms, coping behavior, and alcohol use behavior were assessed with self-report questionnaires. Linear regressions were run to examine whether VS reactivity moderated the relationship between ELS and anhedonic symptoms. Structural equation models examined whether this moderation was indirectly associated with other depression symptoms and problematic alcohol use through its association with anhedonia. Results Analyses of data from 820 participants passing quality control procedures revealed that the VS × ELS interaction was associated with anhedonic symptoms (p = 0.011). Moreover, structural equation models indirectly linked this interaction to non-anhedonic depression symptoms and problematic alcohol use through anhedonic symptoms and substance-related coping. Conclusions These findings suggest that reduced VS reactivity to reward is associated with increased risk for anhedonia in individuals exposed to ELS. Such stress-related anhedonia is further associated with other depressive symptoms and problematic alcohol use through substance-related coping.

Impact of juvenile chronic stress on adult cortico-accumbal function: Implications for cognition and addiction

“…This may be partially explained by likely inherent differences between accumbal responsiveness to drugs of abuse as employed in animal studies, and to the anticipation of monetary-based reward as is typically utilized in human experiments. However, it should be noted that the studies showing blunted accumbal responses to reward following chronic juvenile stress also found that NAc hypoactivity strongly predicted symptoms of anhedonia and depression (Goff et al, 2013; Boecker et al 2014; Corral-Frias et al, 2015; Hanson et al, 2015). Moreover, anhedonia in participants exposed to repeated juvenile stress was linked to problematic alcohol use arising from the use of substances as a coping mechanism (Corral-Frias et al, 2015).…”

“…However, it should be noted that the studies showing blunted accumbal responses to reward following chronic juvenile stress also found that NAc hypoactivity strongly predicted symptoms of anhedonia and depression (Goff et al, 2013; Boecker et al 2014; Corral-Frias et al, 2015; Hanson et al, 2015). Moreover, anhedonia in participants exposed to repeated juvenile stress was linked to problematic alcohol use arising from the use of substances as a coping mechanism (Corral-Frias et al, 2015). Interestingly, hyperactivity of the NAc in response to amphetamine has been reported in individuals who experienced juvenile stress, with the strength of activation being positively correlated with the degree of stress exposure (Oswald et al, 2014).…”

“…In the small number of clinical studies that have examined accumbal function in either human adolescents or adults reporting experiences of repeated social and non-social juvenile stress, hypoactivity of the NAc in response to either reward-related stimuli or reward anticipation is observed (Goff et al, 2013; Boecker et al 2014; Corral-Frias et al, 2015; Hanson et al, 2015, 2016; but see Casement et al, 2014). Initially this would appear to stand in contrast both to the greater incidence of substance abuse disorders seen in victims of childhood stress, and to the increased dopamine activity in the NAc seen in some chronic juvenile stress animal models as discussed above (Table 5).…”

Child trauma exposure and psychopathology: mechanisms of risk and resilience

“…Child trauma is associated with anhedonia less strongly in young adults with high ventral striatum reactivity to reward [43]. Lower levels of anhedonia, in turn, are associated with reduced depression symptoms and problematic drinking following child trauma [43].…”

Toward understanding the impact of trauma on the early developing human brain

“…Structural and functional changes are documented in the dopaminergic reward centers in the brain of animals subjected to early stress (Hall et al, 1999, Chocyk et al, 2015). Further, reduced response to reward in the ventral striatum, a key brain reward center, is documented in early-institutionalized youth (Goff et al, 2013) and adults reporting histories of early stress (Corral-Frías et al, 2015). We and others have found that trauma-related changes in brain function and connectivity correspond with diminished experience of positive affect rather than heightened negative affect (Nikolova et al, 2012, Marusak et al, 2015b), suggesting that robust brain reward function and associated levels of positive affect may be protective against stress-related psychopathology.…”