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神经质与奖赏相关的腹侧纹状体活动:探究与应激相关的抑郁易感性。

Neuroticism and reward-related ventral striatum activity: Probing vulnerability to stress-related depression.

机构信息

Department of Psychological and Brain Sciences.

Department of Psychiatry.

出版信息

J Abnorm Psychol. 2021 Apr;130(3):223-235. doi: 10.1037/abn0000618. Epub 2021 Feb 4.

Abstract

Elevated neuroticism may confer vulnerability to the depressogenic effects of stressful life events (SLEs). However, the mechanisms underlying this susceptibility remain poorly understood. Accumulating evidence suggests that stress-related disruptions in neural reward processing might undergird links between stress and depression. Using data from the Saint Louis Personality and Aging Network (SPAN) study and Duke Neurogenetics Study (DNS), we examined whether neuroticism moderates links between stressful life events (SLE) and depression as well as SLEs and ventral striatum (VS) response to reward. In the longitudinal SPAN sample ( = 971 older adults), SLEs prospectively predicted future depressive symptoms, especially among those reporting elevated neuroticism, even after accounting for prior depressive symptoms and previous SLE exposure (NxSLE interaction: = .016, Δ² = 0.003). Cross-sectional analyses of the DNS, a young adult college sample with neuroimaging data, replicated this interaction ( = 1,343: NxSLE interaction: = .019, Δ² = 0.003) and provided evidence that neuroticism moderates the association between SLEs and reward-related VS response ( = 1,195, NxSLE: = .017, Δ² = 0.0048). Blunted left VS response to reward was associated with a lifetime depression diagnosis, = -0.07, = .02, but not current depressive symptoms, = -0.003, = .93. These data suggest that neuroticism may promote vulnerability to stress-related depression and that sensitivity to stress-related reductions in VS response may be a potential neural mechanism underlying vulnerability to clinically significant depression. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

摘要

神经质水平升高可能使人易患应激性生活事件(SLEs)所致的抑郁。然而,这种易感性的潜在机制仍知之甚少。越来越多的证据表明,与应激相关的神经奖赏处理中断可能是应激与抑郁之间联系的基础。本研究利用圣路易斯人格与衰老网络(SPAN)研究和杜克神经遗传学研究(DNS)的数据,考察了神经质是否调节了应激性生活事件(SLE)与抑郁之间的关系,以及 SLE 与腹侧纹状体(VS)对奖赏的反应之间的关系。在纵向的 SPAN 样本(=971 名老年人)中,SLEs 前瞻性地预测了未来的抑郁症状,尤其是在报告神经质水平升高的人群中,即使考虑了先前的抑郁症状和先前的 SLE 暴露(NxSLE 交互作用:=0.016,Δ²=0.003)。对具有神经影像学数据的年轻成人大学生 DNS 样本的横断面分析复制了这种交互作用(=1343:NxSLE 交互作用:=0.019,Δ²=0.003),并提供了证据表明神经质调节了 SLEs 与奖赏相关的 VS 反应之间的关联(=1195,NxSLE:=0.017,Δ²=0.0048)。左 VS 对奖赏的反应迟钝与终生抑郁诊断有关,= -0.07,=0.02,但与当前的抑郁症状无关,= -0.003,=0.93。这些数据表明,神经质可能会增加与应激相关的抑郁易感性,而对 VS 反应与应激相关降低的敏感性可能是对临床上显著抑郁易感性的潜在神经机制。(PsycInfo 数据库记录(c)2021 APA,保留所有权利)。

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