NEURAL MECHANISMS UNDERLYING STRESS REACTIVITY

应激反应背后的神经机制

• 批准号: 7627643
• 负责人: MATTHEW Dylan LIEBERMAN
• 金额: $ 1万
• 依托单位: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-09-30 至 2008-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7627643
• 关键词: Affect; Amygdaloid structure; Anterior; Biological; Brain; Computer Retrieval of Information on Scientific Projects Database; Funding; Grant; Health; Health Psychology; Human; Hydrocortisone; Immunologics; Individual Differences; Inflammatory; Institution; Investigation; Laboratories; Measures; Mediating; Modeling; Neurocognitive; Neurosecretory Systems; Neurotic Disorders; Participant; Pathway interactions; Pattern; Perception; Physiological; Prefrontal Cortex; Process; Psyche structure; Psychoneuroimmunology; Recovery; Research; Research Personnel; Resources; Risk Factors; Role; Sampling; Source; Stress; Testing; Translating; United States National Institutes of Health; Work; biological adaptation to stress; coping; cytokine; emotion regulation; neuroimaging; neuromechanism; novel; optimism; parent project; psychologic; response; self esteem; social neuroscience

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Research consistently shows that stress negatively affects both mental and physical health. Yet models of stress have thus far not investigated the individual differences in neurocognitive processes that translate perceptions of threat into psychological, physiological, neuroendocrine, and immunological stress responses. That is, no studies to date have examined the complete relationship between the brain's response to threat and the ensuing biological and psychological stress responses, and how these pathways are moderated by key individual differences related to stress reactivity and coping. We hypothesize that the anterior cingulated cortex (ACC) and the amygdala are critically involved in these pathways and that the prefrontal cortex (PFC) regulates the reactivity of this pathway. We will test these relations in the proposed project. In a parent project (MH506880), participants complete individual difference measures of neuroticism, self-esteem, and optimism and participate in a laboratory stress challenge (the TSST), during which autonomic responses, cortisol, and pro-inflammatory cytokines are assessed at baseline, following the stress challenge, and following a recovery period. The current proposal seeks to add a neuroimaging component to this project. We will select a sample of 30 participants from the parent project to complete tasks previously demonstrated to evoke ACC (Cyberball and Go-NoGo tasks) and amygdala (Threat Perception task) activity; as well as PFC activity involved in negative emotion regulation (Cyberball task). We will use these measures to assess whether the magnitude of the ACC, amygdala, and PFC responses is related to individual differences in neuroticism, optimism, and self-esteem and to autonomic, neuroendocrine, and immunologic stress reactivity. We test the predictions that neuroticism will be negatively associated with PFC activity and positively associated with ACC, amygdala, and stress reactivity whereas self-esteem and optimism will show the opposite pattern, correlating positively with PFC activity and negatively with ACC, amygdala, and stress reactivity. Evidence in support of these novel hypotheses will greatly enhance understanding of stress processes and will provide the first investigation in humans of the role of neural mechanisms in mediating the pathway from environmental threat to biological stress reactivity. As such, the proposed work integrates research from health psychology, psychoneuroimmunology, and social neuroscience. Supportive evidence will flesh out the neural mechanisms through which individual differences affect biological responses to stress and elucidate the risk factors for stress- related mental and physical health problems.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 研究一致表明，压力对心理和身体健康都有负面影响。然而，迄今为止，压力模型还没有研究神经认知过程的个体差异，这些过程将威胁的感知转化为心理、生理、神经内分泌和免疫应激反应。也就是说，到目前为止，还没有研究研究大脑对威胁的反应与随后的生物和心理应激反应之间的完整关系，以及这些途径如何受到与应激反应和应对相关的关键个体差异的调节。我们推测，前扣带皮层（ACC）和杏仁核是至关重要的参与这些途径，前额叶皮层（PFC）调节这一途径的反应。我们将在拟议的项目中测试这些关系。在父项目（MH 506880）中，参与者完成神经质、自尊和乐观的个体差异测量，并参与实验室压力挑战（TSST），在此期间，在基线、压力挑战后和恢复期后评估自主神经反应、皮质醇和促炎细胞因子。目前的提案旨在为该项目增加一个神经成像部分。我们将从父项目中选择30名参与者完成先前证明的任务，以唤起ACC（Cyberball和Go-NoGo任务）和杏仁核（威胁感知任务）活动;以及参与消极情绪调节的PFC活动（Cyberball任务）。我们将使用这些措施，以评估是否ACC，杏仁核，PFC反应的幅度与神经质，乐观，自尊和自主神经，神经内分泌和免疫应激反应的个体差异。我们测试的预测，神经质将与PFC活动呈负相关，与ACC，杏仁核和压力反应呈正相关，而自尊和乐观将显示相反的模式，与PFC活动呈正相关，与ACC，杏仁核和压力反应呈负相关。支持这些新假设的证据将大大增强对应激过程的理解，并将首次在人类中研究神经机制在介导从环境威胁到生物应激反应的途径中的作用。因此，拟议的工作整合了健康心理学，心理神经免疫学和社会神经科学的研究。支持性证据将充实个体差异影响对压力的生物反应的神经机制，并阐明与压力相关的心理和身体健康问题的风险因素。