Child Trauma and the Development of Neural Systems Underlying Emotion Regulation

描述（由申请人提供）：童年创伤暴露与儿童、青少年和成人的精神病理发病密切相关，占人口中精神障碍的相当大比例。然而，解释儿童创伤（CT）和精神病理之间关系的神经发育机制仍然缺乏特征。特别是，关于CT如何影响大脑发育的研究仍处于起步阶段。然而，了解由于CT暴露而中断的神经发育过程将提供有关不良环境与精神病理联系途径的关键信息。为此，拟议的项目检查了CT对参与情绪调节的神经网络发展的影响，这是一种将CT与精神病理学联系起来的似是而非的神经生物学途径。拟议的研究通过检查特定类型的早期环境经历——儿童身体或性虐待以及家庭暴力——如何以可能增加精神病理学风险的方式改变神经结构和功能，来解决NIMH战略计划的目标1。我们假设CT暴露会破坏前额叶皮层（PFC）和杏仁核的发育，导致神经功能的非典型模式，并减少这些区域之间的结构和功能连接。我们的目标是通过应用区分情绪反应和内隐和外显情绪调节的神经生物学模型来研究这一假设，从而建立环境经验如何影响负价系统发展的知识。具体来说，我们提出：a) CT暴露导致杏仁核反应性增强，而反应性与创伤严重程度和慢性程度呈正相关；b) CT暴露的慢性程度还与情绪调节缺陷有关，包括PFC对杏仁核反应性的不良调节，这是由于这些区域之间的结构和功能连通性较低造成的。概念模型将通过获取8- 16岁儿童样本的结构和功能MRI数据进行测试；其中一半遭受过儿童虐待或家庭暴力，另一半没有遭受过CT或人际暴力。样本将被招募来确保CT的慢性和严重程度的变化，并允许我们检查CT与神经结构和功能在有或没有预先存在的内在精神病理的儿童中的关联。这项拟议的研究建立在现有研究的基础上，通过研究威胁经历如何影响儿童的神经结构和功能，来研究早期剥夺对大脑发育的影响。研究结果将提供关于CT暴露后情绪反应和调节被破坏的特定方面的关键信息。阐明这些机制不仅将建立关于不良环境如何以可能增加精神病理风险的方式改变神经发育的知识，而且还将为旨在降低暴露于创伤的儿童精神病理风险的预防性干预提供可能的目标。

DESCRIPTION (provided by applicant): Childhood trauma exposure is strongly associated with psychopathology onset in children, adolescents, and adults, accounting for a substantial proportion of mental disorders in the population. However, the neurodevelopmental mechanisms that explain the association between child trauma (CT) and psychopathology remain poorly characterized. In particular, research examining how CT influences brain development remains in its infancy. Yet understanding the neurodevelopmental processes that are disrupted as a result of CT exposure will provide critical information about the pathways linking adverse environments to psychopathology. To that end, the proposed project examines the impact of CT on the development of neural networks involved in emotion regulation, a plausible neurobiological pathway linking CT to psychopathology. The proposed research addresses Objective 1 of the NIMH Strategic Plan by examining how specific types of early environmental experience-child physical or sexual abuse and domestic violence-alter neural structure and function in ways that might increase risk for psychopathology. We hypothesize that CT exposure disrupts the development of the prefrontal cortex (PFC) and amygdala, resulting in atypical patterns of neural function and reduced structural and functional connectivity between these regions. We aim to build knowledge of how environmental experience shapes development in Negative Valence Systems by applying a neurobiological model distinguishing between emotional reactivity and both implicit and explicit emotion regulation to investigate this hypothesis. Specifically, we propose that a) CT exposure leads to heightened amygdala reactivity and that reactivity is positively associated with trauma severity and chronicity, and b) chronicity of exposure to CT is additionally associated with deficits in emotion regulation, involving poor PFC modulation of amygdala reactivity resulting from low structural and functional connectivity between these regions. The conceptual model will be tested by acquiring structural and functional MRI data in a sample of 8- 16 year olds; half with exposure to child maltreatment or domestic violence and half without exposure to CT or interpersonal violence. The sample will be recruited to ensure variation in CT chronicity and severity and to allow us to examine associations of CT with neural structure and function in children with and without pre- existing internalizing psychopathology. The proposed study builds on existing research examining the influence of early deprivation on brain development by examining how experiences of threat influence neural structure and function in children. Study findings will provide critical information regarding the specific aspects of emotional reactivity ad regulation that are disrupted following CT exposure. Elucidating these mechanisms will not only build knowledge of how adverse environments alter neural development in ways that might increase risk for psychopathology, but will also suggest possible targets for preventive interventions aimed at reducing psychopathology risk in children exposed to trauma.