Effects of stress-induced inflammation on reward processing in healthy young women
Effects of stress-induced inflammation on reward processing in healthy young women
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DOI：
10.1016/j.bbi.2019.09.023
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发表时间：
2020-01-01
影响因子：
15.1
通讯作者：
Bower, Julienne E.
中科院分区：
文献类型：
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作者：
Boyle, Chloe C.;Stanton, Annette L.;Bower, Julienne E.
背景：快感缺乏，或丧失兴趣或愉悦感，是精神病理学中抑郁症和跨诊断结构的一个特征。来自临床前模型的理论和令人信服的证据表明，应激性炎症是快感缺乏行为的心理生物学途径；然而，这一途径尚未在人体模型中进行测试。此外，尽管快感缺乏可能反映了奖励的多个维度的失调，但应激性炎症在多大程度上改变了这些维度尚不清楚。因此，本实验研究采用标准化的实验室应激源任务来诱发炎症反应，并评估应激诱导炎症对奖励加工的多种行为指标的影响。方法：健康年轻女性（18-25岁）完成评估奖励学习、动机和敏感性的行为奖励任务，并随机分为急性社会心理应激源组（n = 37）和无应激主动对照组（n = 17）。在应激后90-120分钟重新执行任务，以配合应激诱导炎症反应的高峰。在基线和应激后90和120分钟采集血液样本，评估促炎细胞因子白细胞介素-6 （IL-6）。结果：应激诱导的IL-6与奖励学习过程中反应偏差的增加和获得奖励的可能性较低时动机的增加有关。在动机任务的背景下，对奖励的敏感性与应激诱导的IL-6无关。结论：与假设相反，急性应激后IL-6的轻度升高与奖励学习过程中奖励反应性的增加和动机的选择性增加有关。研究结果有助于将炎症与奖励处理联系起来的新兴和微妙的文献，并证明应激性炎症的行为影响可能在实验室环境中被检测到。
Background: Anhedonia, or loss of interest or pleasure, is a feature of depression and transdiagnostic construct in psychopathology. Theory and compelling evidence from preclinical models implicates stress-induced inflammation as a psychobiological pathway to anhedonic behavior; however, this pathway has not been tested in human models. Further, although anhedonia may reflect dysregulation in multiple dimensions of reward, the extent to which stress-induced inflammation alters these dimensions is unclear. Thus, the current experimental study used a standardized laboratory stressor task to elicit an inflammatory response and evaluate effects of stress-induced inflammation on multiple behavioral indices of reward processing.Methods: Healthy young women (age 18-25) completed behavioral reward tasks assessing reward learning, motivation, and sensitivity and were randomized to undergo an acute psychosocial stressor (n = 37) or a no-stress active control (n = 17). Tasks were re-administered 90-120 min post-stress to coincide with the peak of the stress-induced inflammatory response. Blood samples were collected for assessment of the pro-inflammatory cytokine interleukin-6 (IL-6) at baseline and 90 and 120 min post stressor.Results: Stress-induced IL-6 was associated with increased response bias during reward learning and increased motivation when probability of receiving a reward was low. Sensitivity to reward in the context of a motivation task was not altered in association with stress-induced IL-6.Conclusions: Contrary to hypotheses, mild increases in IL-6 following acute stress were associated with increased reward responsiveness during reward learning and selective increases in motivation. Results contribute to an emerging and nuanced literature linking inflammation to reward processing, and demonstrate that behavioral effects of stress-induced inflammation may be detected in the laboratory setting.