Amygdala and nucleus accumbens activation during reward anticipation moderates the association between life stressor frequency and depressive symptoms.
Amygdala and nucleus accumbens activation during reward anticipation moderates the association between life stressor frequency and depressive symptoms.
复制标题
奖励预期过程中杏仁核和伏隔核的激活调节了生活压力源频率与抑郁症状之间的关联。
DOI：
10.1016/j.jad.2023.02.149
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发表时间：
2023
影响因子：
6.6
通讯作者：
Kaiser,RoselindeH
中科院分区：
文献类型：
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作者：
Fassett-Carman,AlyssaN;Moser,AmeliaD;Ruzic,Luka;Neilson,Chiara;Jones,Jenna;Barnes-Horowitz,Sofia;Schneck,ChristopherD;Kaiser,RoselindeH
研究背景生活压力因素会增加抑郁症状的风险，但个体对生活压力因素的敏感程度不同。一个保护因素可以是个体的奖励敏感度水平，例如，对环境奖励的更强的神经生物学反应可以减轻对压力源的情绪反应。然而，神经生物学的奖励敏感性，对应于压力弹性的性质是未知的。此外，这个模型是未经测试的青春期，当生活压力源的频率和抑郁increases.MethodsWe测试的假设，更强的奖励相关的激活，在左，右丘脑核（NAC），杏仁核，内侧前额叶皮层（mPFC）衰减的强度的压力-抑郁症的关系。我们测量了BOLD在金钱奖励任务的赢和输块中的激活，以及在任务的预期和结果阶段。参与者（N = 151，年龄13 - 19）被招募到分层的情绪障碍的风险，以提高方差在depressive symptoms. ResultsActivation在预期的奖励在双边杏仁核和NAC，但不是mPFC，缓冲生活压力和抑郁症状之间的关联。这种缓冲效应没有发现奖励结果激活或激活跨Win blocks.ConclusionsResults突出奖励预期激活皮层下结构在衰减的压力-抑郁链接的重要性，这表明奖励动机可能是一种认知机制，通过这种压力缓冲发生。
BackgroundLife stressors confer risk for depressive symptoms, but individuals vary in the extent of their sensitivity to life stressors. One protective factor may be an individual's level of reward sensitivity, e.g., a stronger neurobiological response to environmental rewards may mitigate emotional responses to stressors. However, the nature of neurobiological reward sensitivity that corresponds with stress resilience is unknown. Further, this model is untested in adolescence, when life stressor frequency and depression increase.MethodsWe tested the hypothesis that stronger reward-related activation in the left and right nucleus accumbens (NAc), amygdala, and medial prefrontal cortex (mPFC) attenuates the strength of the stress-depression relation. We measured BOLD activation throughout Win and Lose blocks of a monetary reward task, as well as during anticipation and outcome phases of the task. Participants (N= 151, ages 13–19) were recruited to be stratified on risk for mood disorders to enhance variance in depressive symptoms.ResultsActivation during anticipation of rewards in the bilateral amygdala and NAc, but not mPFC, buffered the association between life stressors and depressive symptoms. This buffering effect was not found for reward outcome activation or activation across Win blocks.ConclusionsResults highlight the importance of reward anticipation activation of subcortical structures in attenuating the stress-depression link, suggesting that reward motivation may be a cognitive mechanism through which this stress buffering occurs.