Abstract

Early life stress (ELS) is an important risk factor for the development of depression. Impairments in reward learning and feedback sensitivity are suggested to be an intermediate phenotype in depression aetiology therefore we hypothesised that healthy adults with a history of ELS would exhibit reward processing deficits independent of any current depressive symptoms. We recruited 64 adults with high levels of ELS and no diagnosis of a current mental health disorder and 65 controls. Participants completed the probabilistic reversal learning task and probabilistic reward task followed by depression, anhedonia, social status, and stress scales. Participants with high levels of ELS showed decreased positive feedback sensitivity in the probabilistic reversal learning task compared to controls. High ELS participants also trended towards possessing a decreased model-free learning rate. This was coupled with a decreased learning ability in the acquisition phase of block 1 following the practice session. Neither group showed a reward induced response bias in the probabilistic reward task however high ELS participants exhibited decreased stimuli discrimination. Overall, these data suggest that healthy participants without a current mental health diagnosis but with high levels of ELS show deficits in positive feedback sensitivity and reward learning in the probabilistic reversal learning task that are distinct from depressed patients. These deficits may be relevant to increased depression vulnerability.

Highlights

  • Life stress (ELS) is a major risk factor in the development of depression [1,2,3,4]

  • In the overall reward learning measures of the number of rule changes that participants were able to complete (Fig 1A) and accuracy (Fig 1B) there was no evidence for a difference between no and high Early life stress (ELS) groups

  • In secondary analysis, designed to probe if parameter changes were due to ELS or underlying depression symptomology, there was no evidence of an effect of depression symptomology (RM-ANCOVA, PCA1: p > 0.05) with the main effect of ELS persisting (RM-ANCOVA, ELS: F1,125 = 4.9, p = 0.028)

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Summary

Introduction

Life stress (ELS) is a major risk factor in the development of depression [1,2,3,4]. Elevated levels of childhood stress lead to widespread functional and morphological alterations in the adult brain with the hippocampus, amygdala and prefrontal cortex being most impacted [7,8]. Amongst other functions, these regions are vital mediators of reward learning: the ability of reward in the environment to modulate future behaviour [9,10,11,12,13,14,15,16]. How ELS influences the developing brain to predispose individuals to psychiatric illness is not yet understood [7,17,18].

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