Department of Psychiatry and Behavioral Sciences, Charleston Alcohol Research Center, Center for Drug and Alcohol Programs, 67 President Street, MSC 861, Charleston, SC 29425, USA.
Psychopharmacology (Berl). 2011 Nov;218(1):131-56. doi: 10.1007/s00213-011-2443-9. Epub 2011 Aug 18.
While stress is often proposed to play a significant role in influencing alcohol consumption, the relationship between stress and alcohol is complex and poorly understood. Over several decades, stress effects on alcohol drinking have been studied using a variety of animal models and experimental procedures, yet this large body of literature has generally produced equivocal results.
This paper reviews results from animal studies in which alcohol consumption is evaluated under conditions of acute/sub-chronic stress exposure or models of chronic stress exposure. Evidence also is presented indicating that chronic intermittent alcohol exposure serves as a stressor that consequently influences drinking.
The effects of various acute/sub-chronic stress procedures on alcohol consumption have generally been mixed, but most study outcomes suggest either no effect or decreased alcohol consumption. In contrast, most studies indicate that chronic stress, especially when administered early in development, results in elevated drinking later in adulthood. Chronic alcohol exposure constitutes a potent stressor itself, and models of chronic intermittent alcohol exposure reliably produce escalation of voluntary alcohol consumption.
A complex and dynamic interplay among a wide array of genetic, biological, and environmental factors govern stress responses, regulation of alcohol drinking, and the circumstances in which stress modulates alcohol consumption. Suggestions for future directions and new approaches are presented that may aid in developing more sensitive and valid animal models that not only better mimic the clinical situation, but also provide greater understanding of mechanisms that underlie the complexity of stress effects on alcohol drinking.
尽管压力通常被认为在影响饮酒行为方面起着重要作用，但压力与酒精之间的关系复杂且尚未被充分理解。几十年来，人们使用各种动物模型和实验程序研究了压力对饮酒的影响，但这一大量文献通常得出的结果不一致。
本文综述了在急性/亚慢性应激暴露或慢性应激暴露模型下评估酒精消费的动物研究结果。还提供了证据表明，慢性间歇性酒精暴露作为一种应激源，会影响饮酒。
各种急性/亚慢性应激程序对酒精消费的影响通常不一致，但大多数研究结果表明无影响或酒精消费减少。相比之下，大多数研究表明，慢性应激，特别是在早期发育阶段给予时，会导致成年后期饮酒量增加。慢性酒精暴露本身就是一种强烈的应激源，慢性间歇性酒精暴露模型可可靠地增加自愿饮酒量。
广泛的遗传、生物和环境因素之间复杂而动态的相互作用，控制着应激反应、酒精摄入的调节以及应激调节饮酒的情况。提出了未来的方向和新方法的建议，这可能有助于开发更敏感和有效的动物模型，不仅更好地模拟临床情况，而且更深入地了解应激对饮酒的影响的机制。
