Sleep duration moderates the associations between immune markers and corticolimbic function during stress in adolescents.
Sleep duration moderates the associations between immune markers and corticolimbic function during stress in adolescents.
复制标题
睡眠持续时间调节青少年压力期间免疫标志物与皮质边缘功能之间的关联。
DOI：
10.1016/j.neuropsychologia.2022.108374
复制
发表时间：
2022
期刊：
影响因子：
2.6
通讯作者：
Galván,Adriana
中科院分区：
文献类型：
--
作者：
Uy,JessicaP;Dieffenbach,Macrina;Leschak,CarrianneJ;Eisenberger,NaomiI;Fuligni,AndrewJ;Galván,Adriana
青春期的特点是荷尔蒙和昼夜节律系统的生物学变化，同时伴随着心理社会变化，导致睡眠障碍和压力敏感性增加。在成年人和青少年中，睡眠障碍与高度的压力敏感性和炎症水平有关，但在青少年中，神经相关性尚不清楚。目前的研究调查了外周免疫标记物(IL-6、肿瘤坏死因子-α)的个体差异是否以及如何与青少年对应激的神经反应有关，以及这些免疫与大脑的联系是否受到青少年睡眠时间的影响。符合功能磁共振成像质量控制标准的37名青少年(14-15岁)报告了每天的睡眠时间为7天，并执行了功能磁共振应激源任务。另外，23名青少年的子样本还提供了血液样本，这些样本使用多重分析方法进行了炎症标志物的检测。结果显示，在应激源任务中，平均睡眠时间缓和了肿瘤坏死因子-α和额叶边缘内侧回路(杏仁核、额叶内侧皮质)之间的联系，因此，在报告睡眠时间较短的青少年中，肿瘤坏死因子-α水平较高与压力期间这些区域的更大失活相关，这与更大的自我报告的焦虑有关。这些发现表明，睡眠时间不足加上外周炎症水平较高，可能会促进以应激期间额叶边缘回路改变为特征的神经特征，这可能会加剧睡眠障碍和/或外周炎症。
Adolescence is characterized by biological changes in hormonal and circadian systems that, with concurrent psychosocial changes, result in increased sleep disturbances and stress sensitivity. Sleep disturbance has been associated with heightened stress sensitivity and elevated levels of inflammation in adults and adolescents, yet the neural correlates are unknown in adolescents. The current study investigated whether and how individual differences in peripheral immune markers (IL-6, TNF-α) related to neural response to stress in adolescents and whether these immune-brain associations were moderated by adolescents' sleep duration. Thirty-seven adolescents (14–15 years) who met quality control criteria for fMRI reported daily sleep duration for 7 days and performed a fMRI stressor task. A subsample of 23 adolescents additionally provided blood samples that were assayed for inflammatory markers using a multiplex assay. Results revealed that average sleep duration moderated associations between TNF-α and medial frontolimbic circuitry (amygdala, medial prefrontal cortex) during the stressor task such that, among adolescents who reported shorter sleep duration, higher levels of TNF-α were associated with greater deactivation in those regions during stress, which was associated with greater self-reported anxiety. These findings suggest that insufficient sleep duration coupled with greater levels of peripheral inflammation may promote a neural profile characterized by alterations in frontolimbic circuitry during stress, which can exacerbate sleep disturbances and/or peripheral inflammation.