期刊
BIOLOGICAL PSYCHIATRY
卷 82, 期 8, 页码 570-577出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2017.02.1183
关键词
Inflammation; Interleukin-6; Reinforcement learning; Reward prediction error; Stress; Ventral striatum
资金
- National Institutes of Mental Health [R01, R37 MH068376, MH068376-09S1]
- Brain and Behavior Research Foundation
- Avanir Pharmaceuticals
- NeuroCog
- BlackThorn Therapeutics
- Boston Consulting Group
- Akili Interactive Labs
- Pfizer
- PositScience
- [K99/R00MH102355]
- [R01MH108605]
BACKGROUND: Stress is widely known to alter behavioral responses to rewards and punishments. It is believed that stress may precipitate these changes through modulation of corticostriatal circuitry involved in reinforcement learning and motivation, although the intervening mechanisms remain unclear. One candidate is inflammation, which can rapidly increase following stress and can disrupt dopamine-dependent reward pathways. METHODS: Here, in a sample of 88 healthy female participants, we first assessed the effect of an acute laboratory stress paradigm on levels of plasma interleukin-6 (IL-6), a cytokine known to be both responsive to stress and elevated in depression. In a second laboratory session, we examined the effects of a second laboratory stress paradigm on reward prediction error (RPE) signaling in the ventral striatum. RESULTS: We show that individual differences in stress-induced increases in IL-6 (session 1) were associated with decreased ventral striatal RPE signaling during reinforcement learning (session 2), though there was no main effect of stress on RPE. Furthermore, changes in IL-6 following stress predicted intraindividual variability in perceived stress during a 4-month follow-up period. CONCLUSIONS: Taken together, these data identify a novel link between IL-6 and striatal RPEs during reinforcement learning in the context of acute psychological stress, as well as future appraisal of stressful life events.
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