Prefrontal cortex stimulation normalizes deficient adaptive learning from outcome contingencies in low mood.

IF 5.8 1区 医学 Q1 PSYCHIATRY
Verena Sarrazin, Margot Juliëtte Overman, Luca Mezossy-Dona, Michael Browning, Jacinta O'Shea
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引用次数: 0

Abstract

Depression and anxiety are associated with deficits in adjusting learning behaviour to changing outcome contingencies. This is likely to drive and maintain symptoms, for instance, by perpetuating negative biases or a sense of uncontrollability. Normalising such deficits in adaptive learning might therefore be a novel treatment target for affective disorders. The aim of this experimental medicine study was to test whether prefrontal cortex transcranial direct current stimulation (tDCS) could normalise these aberrant learning processes in depressed mood. To test proof-of-concept, we combined tDCS with a decision-making paradigm that manipulates the volatility of reward and punishment associations. 85 participants with low mood received tDCS during (or before) the task. In two sessions participants received real or sham tDCS in counter-balanced order. Compared to healthy controls (n = 40), individuals with low mood showed significantly impaired adjustment of learning rates to the volatility of loss outcomes. Prefrontal tDCS applied during task performance normalised this deficit, by increasing the adjustment of loss learning rates. As predicted, prefrontal tDCS before task performance (control) had no effect. Thus, the effect was cognitive-state dependent. Our study shows, for the first time, that a candidate depression treatment, prefrontal tDCS, when paired with a task, can reverse deficits in adaptive learning from outcome contingencies in low mood. Thus, combining neurostimulation with a concurrent cognitive manipulation is a potential novel strategy to enhance the effect of tDCS in depression treatment.

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来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
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