Adaptations underlying the development of excessive alcohol intake in selectively bred mice.

Adaptations underlying the development of excessive alcohol intake in selectively bred mice.
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选择性饲养的小鼠出现过量饮酒的适应机制。

DOI:
10.1111/acer.12327
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发表时间:
2014
期刊:
Alcoholism, clinical and experimental research
影响因子:
--
通讯作者:
Kippin,TodE
Kippin,TodE
中科院分区:
--
文献类型:
--
作者:
Kippin,TodE

文献摘要

被引文献

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背景这篇评论讨论了马特森及其同事在本期发表的题为“选择性繁殖的杂交高酒精偏好小鼠饮酒中毒并产生功能性耐受,但在自由选择乙醇的过程中不会发生运动致敏”以及提供对其他药物滥用的研究进行比较。方法对目标文章的结果进行评估,并与更大的文献进行比较。结果在他们的研究中,马特森和同事报告说,小鼠杂交不同的线选择性地培育高酒精摄入量表现出最初的酒精摄入量与运动障碍,其次是消费和耐受性的显着升级酒精对运动协调的影响。相比之下,未观察到酒精诱导运动的药代动力学耐受性或致敏性证据。这些结果表明,cHAP小鼠构成了一个适当的模型,过度饮酒,这是由酒精摄入量和功能的变化,导致过度injuriation.ConclusionsFuture的工作应评估适应的动机过程和主观影响的酒精以及潜在的遗传和表观遗传基础的酒精摄入量的升级。
BackgroundThis commentary discusses the important contributions of the article in this issue by Matson and colleagues entitled “Selectively bred crossed high‐alcohol‐preferring mice drink to intoxication and develop functional tolerance, but not locomotor sensitization during free‐choice ethanol access” as well as providing comparison to studies on other drugs of abuse.MethodsThe findings of the target article are evaluated and compared to the larger literature of intake escalation and vulnerability to addiction observed with other drugs of abuse.ResultsIn their study, Matson and colleagues report that mice derived by crossing different lines selectively bred for high alcohol intake exhibit initial alcohol intakes associated with motor impairment followed by marked escalation of consumption and tolerance to the effects of alcohol on motor coordination. In contrast, no evidence of pharmacokinetic tolerance or sensitization of alcohol‐induced locomotion was observed. These results demonstrate that the cHAP mice constitute an appropriate model for the study of excessive drinking, which is produced by escalated alcohol intake and functional changes, leading to excessive intoxication.ConclusionsFuture work should assess adaptations in motivational processes and subjective effects of alcohol as well as the potential genetic and epigenetic bases of escalated alcohol intake.