Deprivation and Threat: Dimensions of Early Experience and Neural Development

剥夺和威胁：早期经历和神经发育的维度

• 批准号: 9190327
• 负责人: Katie McLaughlin
• 金额: $ 60.54万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-12-10 至 2020-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9190327
• 关键词: Address; Age; Amygdaloid structure; Animal Experimentation; Animals; Area; Biological Neural Networks; Brain; Child; Child Abuse; Childhood; Chronic; Cognitive; Data; Development; Dimensions; Disease; Emotional; Environment; Environmental Exposure; Exposure to; Extinction (Psychology); Failure; Fright; Functional Magnetic Resonance Imaging; Funding; Growth; Knowledge; Learning; Link; Longitudinal cohort; Measures; Mediating; Mental Health; Methods; Modeling; National Institute of Mental Health; Negative Valence; Neurophysiology - biologic function; Neuropsychology; Parietal; Parietal Lobe; Pathway interactions; Performance; Poverty; Prefrontal Cortex; Preventive Intervention; Process; Psychopathology; Research; Risk; Sampling; Severities; Specific qualifier value; Stimulus; Strategic Planning; Structure; Support System; System; Testing; Thick; Time; Trauma; United States National Institutes of Health; abuse neglect; base; cognitive control; conditioned fear; deprivation; design; early childhood; early experience; emotion regulation; experience; neural circuit; neurodevelopment; neuroimaging; novel; public health relevance; relating to nervous system; social; synaptic pruning; white matter

 DESCRIPTION (provided by applicant): Extensive research finds robust links between mental health and childhood adversity (CA), encompassing diverse exposures from child abuse to poverty. Despite the strength and consistency of these findings, the mechanisms producing such links remain poorly specified. In particular, past research has failed to identify how specifi environmental experiences influence specific neural processes. Such limitations arise from the difficulty of precisely quantifying relevant CA and neural variables in children. The current proposal addresses these limitations by capitalizing on a unique, well characterized NIH-funded longitudinal cohort of children where multiple aspects of CA have been precisely assessed and use of rigorous neuroimaging methods to quantify functioning in specific neural circuits. We will use these methods to test a novel conceptual framework delineating how specific types of environmental experience influence specific neural processes, addressing Objective 1 of the NIMH Strategic Plan. Our model argues that different types of CA have distinct effects on neural development. The central distinction we make is between trauma and deprivation. Trauma exposure involves harm or threat of harm, resulting in fear learning mediated by limbic pathways that are well characterized in animals and conserved across species. We argue that child trauma alters development of circuits in the Negative Valence System that support emotional learning encompassing amygdala and ventromedial prefrontal cortex (PFC). In contrast, deprivation involves absence of expected cognitive and social inputs and environmental complexity. Animal research shows that deprivation disrupts development in PFC and parietal cortex by hijacking the typical process of synaptic pruning. Thus we predict that social-cognitive deprivation influences Cognitive Control Systems, resulting in age-specific reductions in thickness and volume of dorsolateral PFC and superior parietal cortex and reduced performance on cognitive control tasks supported by these areas. Clearly, trauma and deprivation are correlated. Our unique design will measure these experiences on separate dimensions informed by rich preliminary data indicating distinct effects of trauma and deprivation on neural development even in samples with high exposure co-occurrence. Our proposed conceptual model will be tested by acquiring structural and functional MRI data on an existing sample of 300 children (1/3 in poverty, 1/3 near poverty, and 1/3 middle class) followed since early childhood with significant variability in CA exposure. Psychopathology has been measured in previous waves of the study and will be collected multiple times during the study period. Study findings will provide critical information about how specific dimensions of environmental experience influence specific neural processes. Elucidating these mechanisms will not only build knowledge of how adverse environments alter neural development in ways that increase risk for psychopathology, but will also suggest possible targets for preventive interventions aimed at reducing psychopathology risk in children exposed to trauma and deprivation.

 描述（由适用提供）：广泛的研究发现心理健康与儿童期广告（CA）之间的牢固联系，包括从虐待儿童到贫困的潜水员暴露。尽管这些发现具有强度和一致性，但产生这种联系的机制仍然很差。特别是，过去的研究未能确定特定的环境经历如何影响特定的神经过程。这种局限性源于精确量化儿童相关的CA和神经变量的困难。当前的提案通过利用独特的，具有良好特征的NIH资助的儿童的纵向同类来解决这些局限性，在该儿童中，CA的多个方面已得到精确评估，并使用了严格的神经影像学方法来量化特定神经记录中的功能。我们将使用这些方法来测试一个新颖的概念框架，描述了特定类型的环境经验如何影响特定的神经源，并解决了NIMH战略计划的目标1。我们的模型认为，不同类型的CA对神经发育有明显的影响。我们的中心障碍是在创伤和剥夺之间。创伤暴露涉及伤害或威胁伤害，导致恐惧学习是由动物中良好特征并构成各种物种的边缘途径所介导的。我们认为，儿童创伤会改变负价系统中电路的发展，该系统支持情绪学习，包括杏仁核和腹膜前额叶皮层（PFC）。相反，剥夺涉及缺乏预期的认知和社会投入以及环境复杂性。动物研究表明，剥夺通过劫持典型的突触修剪过程来破坏PFC和顶叶皮层的发育。我们预测，社会认知剥夺会影响认知控制系统，从而导致年龄特异性的厚度和背外侧PFC和上层顶叶皮质的体积减少，并降低了这些领域支持的认知控制任务的性能。显然，创伤和剥夺是相关的。我们的独特设计将在通过丰富的初步数据所构成的单独维度上衡量这些经验，这些数据表明创伤和剥夺对神经元发展的明显影响，即使在暴露率高的样本中也是如此。自童年以来，我们提出的概念模型将通过在现有的300名儿童（贫困1/3，贫困1/3和1/3中产阶级）的样本上获取结构和功能性MRI数据来测试。精神病理学已经在先前的研究波中进行了测量，并将在研究期间多次收集。研究发现将提供有关环境经验的特定维度如何影响特定神经元过程的关键信息。阐明这些机制不仅会以增加心理病理风险的方式改变神经发育的知识，而且还将提出旨在减少受创伤和剥夺儿童精神病理风险的预防干预措施的可能目标。