fMRI and Integrated Neurocardiac Control of Alcohol Cue Reactivity

此R21应用程序是在响应PA-10-256：行为调节机制， 酒精依赖和相关的表型。在酒精使用障碍患者中， 控制饮酒行为的努力经常被自动化的过程所破坏， 在酒精暗示的背景下吸引注意力并激发唤醒。持续存在 即使在治疗后，提高的线索反应性也对公众健康有重大贡献。 慢性复发性酒精依赖症的负担。线索反应性过程 涉及大脑和其他身体器官（如心脏）之间的动态反馈回路。 然而，很少有人知道大脑和心脏如何共同工作，以提高 酒精提示反应。我们建议通过检查神经心脏反馈来解决这个问题 循环在暴露于酒精图片线索（目标1）。此外，还需要发展 干预措施，有效地减少反应的人，为他们的自动过程，如 因为这些由神经心脏反馈回路支持，保持酒精提示的显著性。因此我们 进一步测试是否短暂的行为操纵可以显着减少神经和 对酒精线索的心血管反应（目标2）。我们将使用功能性磁共振 功能磁共振成像（fMRI）捕捉大脑的中央自主神经网络（CAN）的反应， 同时评估酒精相关的心血管变化， 中性图片线索在一组24个非寻求治疗的新兴成年人与酒精 依赖（DEP）与适度饮酒对照（MOD）的匹配样本相比。 激活选定的CAN结构（内侧前额叶皮层、脑干）， 神经心脏信号变异性（心率变异性和血压变异性） 酒精的影响将同时进行评估。具体目标1将研究 DEP和MOD年轻人之间的酒精提示反应在大脑激活方面，有效 连接和神经心脏信号的生理测量。第2章将探索 以0.1 Hz呼吸的行为操纵是否降低了神经和/或心血管 对酒精的反应如果成功的话，这种应用将为一种新的方法提供支持。 其中神经心脏信号传导可以以时变方式与 调节线索反应性。其潜在的公共卫生意义在于探索一种行为 监管干预，将适合大规模传播，并可用于 在治疗的背景下或在复发的脆弱性增加的时刻即兴。

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.