Life stress in adolescence predicts early adult reward-related brain function and alcohol dependence
Life stress in adolescence predicts early adult reward-related brain function and alcohol dependence
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DOI：
10.1093/scan/nsu061
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发表时间：
2015-03-01
影响因子：
4.2
通讯作者：
Forbes, Erika E.
中科院分区：
文献类型：
--
作者：
Casement, Melynda D.;Shaw, Daniel S.;Forbes, Erika E.
压力性生活事件会增加出现饮酒问题的风险，其作用机制可能是扰乱与奖赏相关的神经回路。这对青少年尤为重要，因为饮酒行为在青春期中期之后急剧增加，酗酒在20岁时达到高峰。与儿童相比，青少年报告的压力源也更多，而且由于前额叶皮质的重塑，神经奖赏回路在青春期可能尤其容易受到压力源的影响。在一项纵向功能性磁共振成像研究中，我们对大量男性参与者（N = 157）进行了研究，评估了15岁至18岁之间累积的压力性生活事件是否与20岁时与奖赏相关的大脑功能以及饮酒问题有关。青春期较高的累积压力性生活事件与在金钱奖赏预期期间以及收到金钱奖赏之后内侧前额叶皮质（mPFC）的反应降低有关。在奖赏预期期间以及奖赏结果出现之后，mPFC反应因压力而降低与酒精依赖的严重程度有关。此外，mPFC反应在压力性生活事件与后来的酒精依赖症状之间起中介作用。这些数据与成瘾的神经生物学模型一致，该模型提出青春期的压力源通过扰乱奖赏回路功能增加了出现饮酒问题的风险。
Stressful life events increase vulnerability to problematic alcohol use, and they may do this by disrupting reward-related neural circuitry. This is particularly relevant for adolescents because alcohol use rises sharply after mid-adolescence and alcohol abuse peaks at age 20. Adolescents also report more stressors compared with children, and neural reward circuitry may be especially vulnerable to stressors during adolescence because of prefrontal cortex remodeling. Using a large sample of male participants in a longitudinal functional magnetic resonance imaging study (N = 157), we evaluated whether cumulative stressful life events between the ages of 15 and 18 were associated with reward-related brain function and problematic alcohol use at age 20 years. Higher cumulative stressful life events during adolescence were associated with decreased response in the medial prefrontal cortex (mPFC) during monetary reward anticipation and following the receipt of monetary rewards. Stress-related decreases in mPFC response during reward anticipation and following rewarding outcomes were associated with the severity of alcohol dependence. Furthermore, mPFC response mediated the association between stressful life events and later symptoms of alcohol dependence. These data are consistent with neurobiological models of addiction that propose that stressors during adolescence increase risk for problematic alcohol use by disrupting reward circuit function.