Aggression and SEIP: Neural Correlates During Alcohol Intoxication

攻击性和 SEIP：酒精中毒期间的神经相关性

• 批准号: 10266858
• 负责人: EMIL Frank COCCARO
• 金额: $ 63.9万
• 依托单位: OHIO STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-09-05 至 2023-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10266858
• 关键词: Acute; Address; Affect; Aggressive behavior; Alcohol consumption; Alcoholic Intoxication; Alcohols; Amygdaloid structure; Behavioral; Brain; Closure by clamp; Cognitive; Complex; Control Groups; Corpus striatum structure; Cues; DSM-V; Data; Dose; Emotional; Equilibrium; Executive Dysfunction; Exercise; Fostering; Functional Magnetic Resonance Imaging; Human; Impairment; Impulsivity; Individual; Infusion procedures; Injury; Intermittent Explosive Disorders; Intervention; Intravenous; Laboratories; Lead; Link; Measures; Methodology; Nature; Neuronal Plasticity; Neurons; Neurosciences; Participant; Pharmacology; Process; Randomized; Recording of previous events; Recurrence; Rehabilitation therapy; Reporting; Risk; Saline; Signal Transduction; Social Environment; Societies; Structure; System; Testing; Ventral Striatum; alcohol abuse therapy; alcohol effect; alcohol free; alcohol misuse; alcohol use disorder; assault; base; blood oxygenation level dependent response; cognitive function; comorbidity; cortico-limbic circuits; functional MRI scan; improved; information processing; insight; life history; neural circuit; neural correlate; neural information processing; neuronal circuitry; non-alcoholic; novel; relating to nervous system; remediation; response; social; social neuroscience; trait; violent crime

Project Summary: The specific aim of this project is to experimentally examine the effect of alcohol on aggressive and impulsive responding, and on social-emotional information processing (SEIP) responses to threat, in individuals as a function of Alcohol Use Disorder (AUD) and prominent history of recurrent, problematic, impulsive aggressive behavior (AGG). While alcohol use is associated with impulsive aggression, little is known about the system neuroscience nature of this association except that the link between alcohol and aggression is most clear, and strongest, in individuals who are already high in trait aggression. Recent reports suggest that history of high lifetime alcohol use, in addition to acute alcohol dosing, dampens both cortical and subcortical responses to threat. In addition, acute alcohol administration appears to reduce cortical-subcortical connectivity, which some suggest is the primary correlate of alcohol-related aggressive behavior. However, this cannot explain all cases of alcohol-related aggression because neuronal correlates of aggression in non-alcoholics include an over, rather than under-activation of subcortical structures (i.e., amygdala) in the alcohol-free state. To advance our understanding of these complex relationships, we propose to study neuronal responses to socio-emotional threat in four groups of subjects: a) AUD and AGG (AUD+AGG); b) AUD without AGG (AUD); c) IED without AUD (AGG); and d) Healthy Controls (AUD-/AGG-), to uncover behavioral and neuro-circuitry differences in impulsive aggression and in the neuronal response to threat as a function of a history of AUD. Specifically, this study proposes to test the hypothesis that alcohol intoxication (0.08 mg%) is associated with increases in aggressive responding, and impairment in measures of SEIP, and to test the hypothesis that alcohol intoxication further affects cortico-limbic function in ways to increase the risk of impulsive aggression, though, perhaps, by different neuronal mechanisms as a function of AUD. Subjects will complete two (2) study sessions, in randomized order, in which each will receive intravenous alcohol (using alcohol clamp methodology), with alcohol doses clamped to achieve steady state alcohol breath levels of 0.08 mg%. Subjects will then complete a human laboratory aggression task and then an fMRI scanning session including two social-emotional information processing tasks: a) one that taps into the processing of explicit emotional cues of threat and, b) one that taps into the processing of ambiguous social cues of threat.

项目摘要：该项目的具体目的是实验检查酒精的影响 积极反应的反应以及对社会情感信息处理（SEIP）对 威胁，在个体中是饮酒障碍（AUD）和重复的重要历史的函数， 有问题的，冲动的攻击行为（AGG）。虽然饮酒与冲动侵略有关 对该关联的神经科学性质知之甚少，除了酒精之间的联系 对于已经很高的性状侵略的个体，侵略是最清晰，最强大的。最近的 报告表明，除了急性酒精剂量外，终身使用量高饮酒的病史都会降低 皮质和皮层对威胁的反应。此外，急性酒精施用似乎减少了 皮质增生的连通性，有些人建议是酒精相关侵略性的主要相关性 行为。但是，这无法解释所有与酒精相关侵略的案例，因为神经元相关 非酒精饮料的侵略包括过度，而不是对皮层结构的激活（即， 无酒精状态的杏仁核）。为了促进我们对这些复杂关系的理解，我们提出 研究四组受试者对社会情感威胁的神经元反应：a）AUD和AGG （aud+agg）; b）无agg（aud）aud; c）没有aud（agg）的IED； d）健康对照（aud-/agg-）， 发现冲动攻击和神经元反应的行为和神经通路差异 威胁是AUD历史的函数。具体而言，这项研究提出了测试酒精的假设 中毒（0.08毫克％）与侵略性反应的增加有关，措施的损害 seip，并检验以下假设：酒精中毒进一步影响皮质膜功能 但是，也许通过不同的神经元机制增加冲动侵略的风险 奥德受试者将以随机顺序完成两个（2）个学习课程，其中每个人都会收到 静脉酒精（使用酒精夹方法），酒精剂量夹紧以达到稳态 酒精呼吸水平为0.08 mg％。然后，受试者将完成人类实验室侵略任务，然后 fMRI扫描会议，包括两个社会情感信息处理任务：a）一项攻击 处理威胁的明确情感线索，b）涉及模棱两可的处理 威胁的社会线索。