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.

项目概述：本项目的具体目标是通过实验研究酒精对 攻击性和冲动性反应，以及社会情绪信息处理（SEIP）反应， 威胁，在个人中作为酒精使用障碍（AUD）和复发的突出历史的函数， 冲动性攻击行为（Impulsive aggressive behavior，AGG）虽然饮酒与冲动性攻击有关， 除了酒精之间的联系之外，人们对这种联系的系统神经科学性质知之甚少 而攻击性在那些已经具有高特质攻击性的个体中是最明显、最强烈的。最近 报告表明，除了急性酒精剂量外，一生中大量饮酒的历史， 皮层和皮层下对威胁的反应此外，急性酒精摄入似乎减少了 皮质-皮质下连接，有些人认为这是酒精相关的攻击性的主要相关因素。 行为然而，这并不能解释所有与酒精有关的攻击性病例，因为神经元相关的 非酗酒者的攻击性包括皮质下结构的过度激活，而不是激活不足（即， 杏仁核）在无酒精状态下。为了加深我们对这些复杂关系的理解，我们建议 研究四组受试者对社会情绪威胁的神经元反应：a）AUD和AGG (AUD+AGG）; B）AUD无AGG（AUD）; c）IED无AUD（AGG）;和d）健康对照（AUD-/AGG-）， 揭示冲动性攻击行为和神经回路的差异， 威胁作为澳元历史的函数。具体来说，这项研究提出了测试的假设，酒精 中毒（0.08 mg%）与攻击性反应的增加有关， SEIP，并检验酒精中毒进一步影响皮质边缘功能的假设， 增加冲动性攻击的风险，虽然，也许，通过不同的神经机制， 澳元。受试者将以随机顺序完成两（2）个研究阶段，每个阶段将接受 静脉注射酒精（使用酒精钳夹方法），酒精剂量被钳夹以达到稳态 酒精呼气浓度为0.08mg %。然后，受试者将完成人类实验室攻击任务， 一个功能磁共振成像扫描会议，包括两个社会情绪信息处理任务：a）一个是利用 B）一个是对威胁的明确情感线索的处理，另一个是对模糊情感线索的处理。 威胁的社会线索