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通过实验检查酒精对人体的影响。 攻击性和冲动性反应，以及社交情感信息处理（SEIP）反应 威胁，在个体中作为酒精使用障碍（AUD）和显着的复发病史的函数， 有问题的、冲动的攻击行为（AGG）。虽然饮酒与冲动攻击有关， 除了酒精与酒精之间的联系外，人们对这种关联的系统神经科学性质知之甚少。 在攻击性特质已经很高的个体中，攻击性最为明显、最强。最近的 报告表明，除了急性饮酒之外，终生大量饮酒的历史也会抑制两者 皮质和皮质下对威胁的反应。此外，急性饮酒似乎会减少 皮质-皮质下连接，一些人认为这是与酒精相关的攻击性行为的主要相关性 行为。然而，这并不能解释所有与酒精相关的攻击行为，因为神经元与 非酗酒者的攻击性包括皮层下结构的过度激活，而不是激活不足（即， 杏仁核）处于无酒精状态。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 （澳元+总收益）； b) 不含 AGG 的澳元 (AUD)； c) 不含 AUD 的简易爆炸装置 (AGG)； d) 健康控制（AUD-/AGG-）， 揭示冲动攻击和神经元反应中的行为和神经回路差异 威胁作为澳元历史的函数。具体来说，本研究旨在检验以下假设：酒精 中毒（0.08 mg%）与攻击性反应的增加以及测量指标的损害有关 SEIP，并检验酒精中毒进一步影响皮质边缘功能的假设 增加冲动攻击的风险，尽管可能是通过不同的神经元机制作为函数 澳元。受试者将按随机顺序完成两 (2) 个研究课程，其中每个人都将收到 静脉注射酒精（使用酒精钳法），限制酒精剂量以达到稳态 呼气酒精浓度为 0.08 mg%。然后受试者将完成人类实验室攻击任务，然后 功能磁共振成像扫描会话包括两项社交情感信息处理任务：a）一项利用 b) 处理明确的威胁情绪线索，以及 b) 处理模糊的情绪线索 威胁的社会线索。