Child Trauma and the Development of Neural Systems Underlying Emotion Regulation

描述（由申请人提供）：儿童期创伤暴露与儿童、青少年和成人的精神病理学发作密切相关，占人群中精神障碍的很大比例。然而，解释儿童创伤（CT）和精神病理学之间的关联的神经发育机制仍然很差的特点。特别是，研究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将不利环境与精神病理学联系起来的途径的关键信息。为此，拟议的项目探讨了CT对参与情绪调节的神经网络发展的影响，这是一条将CT与精神病理学联系起来的合理神经生物学途径。拟议的研究通过研究特定类型的早期环境经验-儿童身体或性虐待和家庭暴力-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暴露破坏了前额叶皮层（PFC）和杏仁核的发育，导致神经功能的非典型模式和这些区域之间的结构和功能连接减少。我们的目标是建立知识的环境经验如何塑造负价系统的发展，通过应用神经生物学模型区分情绪反应和内隐和外显的情绪调节来研究这一假设。具体而言，我们提出：a）CT暴露导致杏仁核反应性升高，且该反应性与创伤严重程度和慢性程度呈正相关; B）长期暴露于CT还与情绪调节缺陷相关，涉及这些区域之间结构和功能连接性低导致的杏仁核反应性PFC调节不良。将通过获取8- 16奥尔兹样本的结构和功能MRI数据来测试概念模型;一半儿童遭受虐待或家庭暴力，另一半儿童没有遭受CT或人际暴力。将招募样本以确保CT慢性和严重程度的变化，并允许我们检查有和没有预先存在内在精神病理学的儿童中CT与神经结构和功能的关联。这项研究建立在现有的研究基础上，通过研究威胁的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。研究结果将提供关键信息的具体方面的情绪反应广告调节被破坏后，CT曝光。阐明这些机制不仅将建立知识的不利环境如何改变神经发育的方式，可能会增加精神病理学的风险，但也将建议可能的目标，旨在减少儿童暴露于创伤的精神病理学风险的预防性干预措施。

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.