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童年期虐待会改变化学感应应激信号的神经处理过程。

Childhood Maltreatment Alters the Neural Processing of Chemosensory Stress Signals.

作者信息

Maier Ayline, Heinen-Ludwig Luca, Güntürkün Onur, Hurlemann René, Scheele Dirk

机构信息

Division of Medical Psychology, Department of Psychiatry and Psychotherapy, University Hospital Bonn, Bonn, Germany.

Department of Psychology, Laboratory for Biological Psychology, Ruhr-University of Bochum, Bochum, Germany.

出版信息

Front Psychiatry. 2020 Aug 6;11:783. doi: 10.3389/fpsyt.2020.00783. eCollection 2020.

DOI:10.3389/fpsyt.2020.00783
PMID:32848947
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7425696/
Abstract

Accumulating evidence suggests that childhood maltreatment (CM) confers risk for psychopathology later in life by inducing hypervigilance to social threat cues such as fearful faces. However, it remains unclear whether the modulatory impact of CM extents to the olfactory domain of social communication in humans. To address this question, we examined whether CM modulates the neural processing of chemosensory threat signals in sweat and whether CM affects the stress-reducing effects of oxytocin (OXT) in this context. In a randomized, double-blind within-subject functional MRI study design, 58 healthy participants (30 females) received intranasal OXT (40 IU) or placebo (PLC) and completed a forced-choice emotion recognition task with faces of varying emotion intensities (neutral to fearful) while exposed to sweat stimuli and a non-social control odor. Axillary sweat samples were collected from 30 healthy male donors undergoing an acute psychosocial stressor (stress) and ergometer training (sport) as control in a pre-study. CM was assessed by the 25-item Childhood Trauma Questionnaire (CTQ). The final fMRI analysis included 50 healthy participants (26 females). Regression analysis showed a stress-specific association of CTQ scores with amygdala hyperreactivity, hippocampal deactivation, and increased functional connectivity between the amygdala and the hippocampus, medial orbitofrontal cortex, and the anterior cingulate cortex (ACC) under PLC. Furthermore, we observed a positive association of CTQ scores and the dampening effects of OXT on stress-related amygdala responses. Our findings suggest that CM may induce hypervigilance to chemosensory threat cues in a healthy sample due to inefficient frontolimbic inhibition of amygdala activation. Future studies should investigate whether increased recruitment of the intralimbic amygdala-hippocampus complex reflects a compensatory mechanism that prevents the development of psychopathology in those who have experienced CM. Furthermore, the results reveal that the stress-specific effects of OXT in the olfactory domain are more pronounced in participants with increasing levels of CM exposure.

摘要

越来越多的证据表明,童年期虐待(CM)通过诱导对诸如恐惧面孔等社会威胁线索的过度警觉,使人在日后生活中面临精神病理学风险。然而,CM的调节作用是否扩展到人类社会交流的嗅觉领域仍不清楚。为了解决这个问题,我们研究了CM是否调节汗液中化学感觉威胁信号的神经处理,以及在这种情况下CM是否影响催产素(OXT)的减压效果。在一项随机、双盲的受试者内功能磁共振成像研究设计中,58名健康参与者(30名女性)接受鼻内OXT(40 IU)或安慰剂(PLC),并在暴露于汗液刺激和非社交对照气味的同时,完成一项对不同情绪强度(从中性到恐惧)面孔的强制选择情绪识别任务。在一项前期研究中,从30名经历急性心理社会应激源(应激)和测力计训练(运动)作为对照的健康男性供体中收集腋窝汗液样本。通过25项儿童创伤问卷(CTQ)评估CM。最终的功能磁共振成像分析纳入了50名健康参与者(26名女性)。回归分析显示,在PLC条件下,CTQ评分与杏仁核反应过度、海马失活以及杏仁核与海马、内侧眶额皮质和前扣带回皮质(ACC)之间功能连接增加存在应激特异性关联。此外,我们观察到CTQ评分与OXT对应激相关杏仁核反应的抑制作用呈正相关。我们的研究结果表明,由于额叶边缘系统对杏仁核激活的抑制效率低下,CM可能会在健康样本中诱导对化学感觉威胁线索的过度警觉。未来的研究应调查边缘内杏仁核 - 海马复合体招募增加是否反映了一种补偿机制,该机制可防止经历过CM的人出现精神病理学。此外,结果显示,在CM暴露水平不断增加的参与者中,OXT在嗅觉领域的应激特异性作用更为明显。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/27873fc27cab/fpsyt-11-00783-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/c4cc69cca923/fpsyt-11-00783-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/2890ec5567a6/fpsyt-11-00783-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/98ba91e50310/fpsyt-11-00783-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/27873fc27cab/fpsyt-11-00783-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/c4cc69cca923/fpsyt-11-00783-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/2890ec5567a6/fpsyt-11-00783-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/98ba91e50310/fpsyt-11-00783-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52d8/7425696/27873fc27cab/fpsyt-11-00783-g004.jpg

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