Stress enhancement of craving during sobriety:: A risk for relapse
Stress enhancement of craving during sobriety:: A risk for relapse
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DOI：
10.1097/01.alc.0000153544.83656.3c
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发表时间：
2005-02-01
影响因子：
3.2
通讯作者：
Weiss, F
中科院分区：
文献类型：
--
作者：
Breese, GR;Chu, K;Weiss, F
在2004年酒精中毒研究协会会议上提交的一份研讨会会议记录的这份报告提供了将清醒期间的压力与增加复发风险的渴望联系起来的证据。Rajita Sinha的初步报告总结了酗酒者对压力引起的渴望的敏感性增加这一假设的临床证据。在早期戒酒，酗酒者谁面临着压力的情况下表现出增加复发的易感性。乔治布里斯提供的数据表明，压力可以取代反复从慢性乙醇中提取，以诱导类似焦虑的行为。这种由多次戒断引起的持续适应性变化使压力能够诱导焦虑样反应，而这种反应在以前未暴露于慢性乙醇的动物中是不存在的。随后，阿曼达·罗伯茨回顾了由压力引起的饮酒增加依赖于促肾上腺皮质激素释放因子（CRF）的证据。此外，在长期禁欲期间受到压力的大鼠表现出焦虑样行为，这也依赖于CRF。克里斯托弗·达亚斯指出，压力会增加与酒精有关的线索的恢复。此外，这种影响被先前的酒精依赖所增强。这些压力和酒精相关的环境刺激之间的相互作用依赖于同时激活内源性阿片和CRF系统。AD U涵盖的信息表明，压力促进恢复酒精反应，并总结了多重剥夺对这种相互作用的影响。大卫奥弗斯特里特提供的证据表明，在重复的酒精剥夺期间，约束压力增加了偏好酒精（P）的大鼠的自愿饮酒，导致戒断诱导的焦虑，这在没有压力的情况下是没有观察到的。对压力诱导的自愿饮酒的药物测试表明，5-羟色胺和CRF参与了致敏反应。总的来说，这些发言提供了令人信服的支持，压力参与复发和持续酗酒的原因，并建议新的药理学方法治疗复发引起的压力。
This report of the proceedings of a symposium presented at the 2004 Research Society on Alcoholism Meeting provides evidence linking stress during sobriety to craving that increases the risk for relapse. The initial presentation by Rajita Sinha summarized clinical evidence for the hypothesis that there is an increased sensitivity to stress-induced craving in alcoholics. During early abstinence, alcoholics who were confronted with stressful circumstances showed increased susceptibility for relapse. George Breese presented data demonstrating that stress could substitute for repeated withdrawals from chronic ethanol to induce anxiety-like behavior. This persistent adaptive change induced by multiple withdrawals allowed stress to induce an anxiety-like response that was absent in animals that were not previously exposed to chronic ethanol. Subsequently, Amanda Roberts reviewed evidence that increased drinking induced by stress was dependent on corticotropin-releasing factor (CRF). In addition, rats that were stressed during protracted abstinence exhibited anxiety-like behavior that was also dependent on CRF. Christopher Dayas indicated that stress increases the reinstatement of an alcohol-related cue. Moreover, this effect was enhanced by previous alcohol dependence. These interactive effects between stress and alcohol-related environmental stimuli depended on concurrent activation of endogenous opioid and CRF systems. A.D. U covered information that indicated that stress facilitated reinstatement to alcohol responding and summarized the influence of multiple deprivations on this interaction. David Overstreet provided evidence that restraint stress during repeated alcohol deprivations increases voluntary drinking in alcohol-preferring (P) rats that results in withdrawal-induced anxiety that is not observed in the absence of stress. Testing of drugs on the stress-induced voluntary drinking implicated serotonin and CRF involvement in the sensitized response. Collectively, the presentations provided convincing support for an involvement of stress in the cause of relapse and continuing alcohol abuse and suggested novel pharmacological approaches for treating relapse induced by stress.