fMRI and Integrated Neurocardiac Control of Alcohol Cue Reactivity

此R21应用程序响应PA-10-256：的行为调节机制 酒精依赖及其相关表型。在酒精使用障碍患者中，有意识的 规范饮酒行为的尝试往往受到自动过程的破坏，这些过程 在酒精暗示的背景下，吸引注意力并激起性欲。坚持不懈的 即使在治疗后，线索反应性的增强也对公共健康有很大贡献 慢性、复发性酒精依赖障碍的负担。提示反应过程 涉及大脑和其他身体器官(如心脏)之间的动态反馈循环。 然而，关于大脑和心脏是如何协同工作以产生高度兴奋的知之甚少。 酒精提示反应性。我们建议通过检查神经心脏反馈来解决这个问题。 暴露在酒精图片线索中的循环(目标1)。此外，仍有必要发展 干预措施有效地减少了自动过程的人的反应性，例如 作为神经心脏反馈环的支持，保持酒精提示的显着性。因此，我们 进一步测试一个简短的行为操作是否可以显著降低神经和 心血管对酒精提示的反应性(目标2)。我们将使用功能磁共振 成像(FMRI)捕捉大脑中央自主神经网络(CAN)的反应性，同时 同时评估在呈现酒精相关和 24名未接受治疗的成年酒精中毒患者的中性图片提示 与中度饮酒对照组(MOD)的匹配样本进行比较。 选定的CAN结构(内侧前额叶皮质、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)的响应 对酒精暗示的反应将同时进行评估。具体目标1将考察以下方面的差异 酒精提示反应在DEP和MOD年轻人大脑激活方面的作用，有效 连通性和神经心脏信号的生理测量。《特定目标2》将探索 以0.1赫兹的频率呼吸的行为操作是否会降低神经和/或心血管 对酒精暗示的反应性。如果成功，该应用程序将产生对新方法的支持 其中，神经心脏信号可以以时变的方式链接到 调节球杆的反应性。它潜在的公共卫生意义在于探索一种行为 易于大规模传播并可利用的监管干预措施 在治疗背景下或在复发风险增加的时刻临时采取行动。

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.