fMRI and Integrated Neurocardiac Control of Alcohol Cue Reactivity

酒精提示反应的功能磁共振成像和综合神经心脏控制

基本信息

批准号：
8794390
负责人：
MARSHA E. BATES
金额：
$ 21.61万
依托单位：
RUTGERS, THE STATE UNIV OF N.J.
依托单位国家：
美国
项目类别：
财政年份：
2014
资助国家：
美国
起止时间：
2014-02-01 至 2017-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8794390
关键词：
Activation Analysis Address Affect Alcohol consumption Alcohol dependence Alcohols Area Arousal Attention Back Behavior Control Behavior Therapy Behavioral Biological Neural Networks Blood Pressure Brain Brain Stem Brain imaging Brain region Breathing Cardiovascular system Chronic Cognitive Conscious Cues Data Dependence Disease Electrocardiogram Emotional Environment Feedback Functional Magnetic Resonance Imaging Goals Graph Health Heart Heart Rate Human Insula of Reil Intervention Knowledge Learning Link Magnetic Resonance Imaging Measures Medial Mediating Organ Participant Pathway interactions Persons Phenotype Physiological Prefrontal Cortex Process Public Health Randomized Regulation Relapse Relative (related person)Research Respiration Sampling Signal Transduction Smell Perception Stream Structure System Testing Time Visceral Vision Work afferent nerve alcohol cue alcohol exposure alcohol relapse alcohol response alcohol seeking behavior alcohol use disorder base blood oxygenation level dependent response craving cue reactivity drinking drinking behavior emerging adult experience feeding flexibility heart rate variability neurotransmission novel novel strategies relating to nervous system response visual control young adult

项目摘要

DESCRIPTION (provided by applicant): This R21 application is in response to PA-10-256: Behavioral Regulation Mechanisms of Alcohol Dependence and Related Phenotypes. In persons with alcohol use disorders, conscious attempts to regulate drinking behavior are often undermined by automatic processes that capture attention and instigate arousal in the context of alcohol cues. The persistence of heightened cue reactivity, even following treatment, contributes significantly to the public health burden of the chronic, relapsing disorder of alcohol dependence. Cue reactivity processes involve dynamic feedback loops between the brain and other bodily organs such as the heart. Yet, very little is known about how the brain and heart work together to give rise to heightened alcohol cue reactivity. We propose to address this gap by examining the neurocardiac feedback loop during exposure to alcohol picture cues (Aim 1). Further, there remains a need to develop interventions that effectively diminish reactivity in persons for whom automatic processes, such as those supported by the neurocardiac feedback loop, maintain alcohol cue salience. Thus, we further test whether a brief behavioral manipulation can significantly diminish neural and cardiovascular reactivity to alcohol cues (Aim 2). We will use functional magnetic resonance imaging (fMRI) to capture reactivity of the brain's central autonomic network (CAN) while simultaneously assessing cardiovascular changes during presentation of alcohol-related and neutral picture cues in a group of 24 non-treatment seeking emerging adults with alcohol dependence (DEP) compared to a matched sample of moderate drinking controls (MOD). Activation in selected CAN structures (medial prefrontal cortex, insula, brain stem) and neurocardiac signal variability (heart rate variability and blood pressure variability) in response to alcohol cues will be simultaneously assessed. Specific Aim 1 will examine differences in alcohol cue reactivity between DEP and MOD young adults in terms of brain activation, effective connectivity, and physiological measures of neurocardiac signaling. Specific Aim 2 will explore whether a behavioral manipulation of breathing at 0.1 Hz reduces neural and/or cardiovascular reactivity to alcohol cues. If successful, this application will yield support for a new approach wherein neurocardiac signaling can be linked in a time-varying manner to neural systems that modulate cue reactivity. Its potential public health significance is in exploring a behavioral regulation intervention that would be amenable to large scale dissemination and could be used within the treatment context or ad lib during moments of heightened vulnerability to relapse.

描述（由申请人提供）：此 R21 申请是对 PA-10-256：酒精依赖和相关表型的行为调节机制的回应。对于患有酒精使用障碍的人来说，有意识地尝试调节饮酒行为常常会受到在酒精暗示的背景下吸引注意力和激发兴奋的自动过程的破坏。即使在治疗后，提示反应性的持续增强也会严重加重慢性、复发性酒精疾病的公共卫生负担依赖性。提示反应过程涉及大脑和其他身体器官（例如心脏）之间的动态反馈回路。然而，人们对大脑和心脏如何协同工作以提高酒精提示反应性知之甚少。我们建议通过检查暴露于酒精图片线索期间的神经心脏反馈回路来解决这一差距（目标 1）。此外，仍然需要开发有效减少自动过程（例如由神经心脏反馈回路支持的那些）的人的反应性的干预措施，以维持酒精提示的显着性。因此，我们进一步测试短暂的行为操纵是否可以显着降低神经和心血管对酒精暗示的反应（目标 2）。我们将使用功能磁共振成像 (fMRI) 来捕获大脑中枢自主网络 (CAN) 的反应性，同时评估 24 名未接受治疗的饮酒新兴成年人在呈现与酒精相关和中性图片线索期间的心血管变化。依赖性（DEP）与适度饮酒对照（MOD）的匹配样本进行比较。将同时评估选定的 CAN 结构（内侧前额叶皮层、脑岛、脑干）和神经心脏信号变异性（心率变异性和血压变异性）对酒精提示的反应。具体目标 1 将检查 DEP 和 MOD 年轻人之间酒精提示反应性在大脑激活、有效连接和神经心脏信号传导生理测量方面的差异。具体目标 2 将探讨 0.1 Hz 呼吸的行为控制是否会降低神经和/或心血管对酒精暗示的反应。如果成功，该应用程序将产生支持一种新方法，其中神经心脏信号传导可以以随时间变化的方式与调节提示反应性的神经系统联系起来。其潜在的公共卫生意义在于探索一种行为调节干预措施，该干预措施适合大规模传播，并且可以在治疗背景下使用，也可以在容易复发的时刻随意使用。