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Conceptualizing withdrawal-induced escalation of alcohol self-administration as a learned, plasticity-dependent process

机译:将戒断诱发的酒精自我管理升级概念化为学习的,可塑性依赖的过程

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摘要

This article represents one of five contributions focusing on the topic " Plasticity and neuroadaptive responses within the extended amygdala in response to chronic or excessive alcohol exposure" that were developed by awardees participating in the Young Investigator Award Symposium at the " . Alcoholism and Stress: A Framework for Future Treatment Strategies" conference in Volterra, Italy on May 3-6, 2011 that was organized/chaired by Drs. Antonio Noronha and Fulton Crews and sponsored by the National Institute on Alcohol Abuse and Alcoholism. This review discusses the dependence-induced neuroadaptations in affective systems that provide a basis for negative reinforcement learning and presents evidence demonstrating that escalated alcohol consumption during withdrawal is a learned, plasticity-dependent process. The review concludes by identifying changes within extended amygdala dynorphin/kappa-opioid receptor systems that could serve as the foundation for the occurrence of negative reinforcement processes. While some evidence contained herein may be specific to alcohol dependence-related learning and plasticity, much of the information will be of relevance to any addictive disorder involving negative reinforcement mechanisms. Collectively, the information presented within this review provides a framework to assess the negative reinforcing effects of alcohol in a manner that distinguishes neuroadaptations produced by chronic alcohol exposure from the actual plasticity that is associated with negative reinforcement learning in dependent organisms.
机译:这篇文章代表了五个主题之一,这些主题集中在“年轻的研究者奖研讨会”上的获奖者在“杏仁核内对可塑性和神经适应性反应对慢性或过量酒精暴露的反应”中。酒精中毒和压力:A 2011年5月3日至6日在意大利沃尔泰拉举行的“未来治疗策略框架”会议由Dr.安东尼奥·诺罗尼亚(Antonio Noronha)和富尔顿·克鲁斯(Fulton Crews),并由国家酒精滥用和酒精中毒研究所赞助。这篇综述讨论了情感系统中依赖引起的神经适应,为负强化学习提供了基础,并提供了证据表明戒断期间饮酒量的增加是学习的,可塑性依赖的过程。审查的结论是确定杏仁核强啡肽/κ阿片类药物受体系统的扩展,这些变化可作为发生负强化过程的基础。尽管此处包含的一些证据可能是与酒精依赖相关的学习和可塑性所特有的,但许多信息将与涉及负强化机制的任何成瘾性疾病有关。总体而言,本综述中提供的信息提供了一种评估酒精的负面强化作用的框架,该方式将慢性酒精暴露产生的神经适应与与依赖生物体中的负面强化学习相关的实际可塑性区分开来。

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