Mood Brain and Development Unit, Emotion and Development Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland; Department of Child and Adolescent Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Section on Development and Affective Neuroscience, Emotion and Development Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland.
Biol Psychiatry Cogn Neurosci Neuroimaging. 2019 Oct;4(10):893-901. doi: 10.1016/j.bpsc.2019.05.012. Epub 2019 Jun 3.
Aberrations in both neural reward processing and stress reactivity are associated with increased risk for mental illness; yet, how these two factors relate to each other remains unclear. Several studies suggest that stress exposure impacts reward function, thus increasing risk for psychopathology. However, the alternative hypothesis, in which reward dysfunction impacts stress reactivity, has been rarely examined. The current study aimed to test both hypotheses using a longitudinal design.
Participants were 38 children (23 girls; 61%) from a prospective cohort study. A standard stress-exposure measure was collected at 7 years of age. Children performed a well-validated imaging reward paradigm at age 10, and a standardized acute psychological stress laboratory protocol was administered both at age 10 and at age 13. Structural equation modeling was used to examine bidirectional associations between stress and neural response to reward anticipation.
Higher exposure to stressful life events at age 7 predicted lower neural response to reward anticipation in regions of the basal ganglia at age 10, which included ventral caudate, nucleus accumbens, putamen, and globus pallidus. Lower response to reward anticipation in medial prefrontal and anterior cingulate cortex predicted higher stress reactivity at age 13.
Our findings provide support for bidirectional associations between stress and reward processing, in that stress may impact reward anticipation, but also in that reduced reward anticipation may increase susceptibility to stress.
神经奖励处理和应激反应的异常与精神疾病的风险增加有关;然而,这两个因素如何相互关联尚不清楚。有几项研究表明,应激暴露会影响奖励功能,从而增加精神病理学的风险。然而,奖励功能障碍影响应激反应的相反假设很少被检验。本研究旨在使用纵向设计来检验这两种假设。
参与者是来自前瞻性队列研究的 38 名儿童(23 名女孩,占 61%)。在 7 岁时收集了一项标准的应激暴露测量。儿童在 10 岁时进行了一项经过充分验证的成像奖励范式,并且在 10 岁和 13 岁时都进行了标准化的急性心理应激实验室方案。结构方程模型用于检验应激和奖励预期神经反应之间的双向关联。
7 岁时更高的生活应激事件暴露预测了 10 岁时基底神经节区域奖励预期的神经反应降低,其中包括腹侧尾状核、伏隔核、壳核和苍白球。内侧前额叶和前扣带回皮层的奖励预期反应降低预测了 13 岁时应激反应性增加。
我们的研究结果支持应激和奖励处理之间的双向关联,即应激可能影响奖励预期,但也表明减少奖励预期可能会增加对应激的易感性。