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酒精滥用动机的遗传贡献的啮齿动物模型。

Rodent models of genetic contributions to motivation to abuse alcohol.

作者信息

Crabbe John C

出版信息

Nebr Symp Motiv. 2014;61:5-29. doi: 10.1007/978-1-4939-0653-6_2.

Abstract

In summary, there are remarkably few studies focused on the genetic contributions to alcohol's reinforcing values. Almost all such studies examine the two-bottle preference test. Despite the deficiencies I have raised in its interpretation, a rodent genotype's willingness to drink ethanol when water is freely available offers a reasonable aggregate estimate of alcohol's reinforcing value relative to other genotypes (Green and Grahame 2008). As indicated above, however, preference drinking studies will likely never avoid the confounding role of taste preferences and most often yield intake levels not sufficient to yield a pharmacologically significant BAL. Thus, the quest for improved measures of reinforcing value continues. Of the potential motivational factors considered by McClearn in his seminal review in this series, we can safely conclude that rodent alcohol drinking is not primarily directed at obtaining calories. The role of taste (and odor) remains a challenge. McClearn appears to have been correct that especially those genotypes that avoid alcohol are probably doing so based on preingestive sensory cues; however, postingestive consequences are also important. Cunningham's intragastric model shows the role of both preingestional and postingestional modulating factors for the best known examples, the usually nearly absolutely alcohol-avoiding DBA/2J and HAP-2 mice. Much subsequent data reinforce McClearn's earlier conclusion that C57BL/6J mice, at least, do not regulate their intake around a given self-administered dose of alcohol by adjusting their intake. This leaves us with the puzzle of why nearly all genotypes, even those directionally selectively bred for high voluntary intake for many generations, fail to self-administer intoxicating amounts of alcohol. Since McClearn's review, many ingenious assays to index alcohol's motivational effects have been used extensively, and new methods for inducing dependence have supplanted the older ones prevalent in 1968. I have tried to identify promising areas where the power of genetics could be fruitfully harvested and generally feel that we have a much more clear idea now about some important experiments remaining to be performed.

摘要

总之,关注基因对酒精强化价值影响的研究非常少。几乎所有此类研究都采用双瓶偏好试验。尽管我对该试验的解读提出了诸多不足,但当有自由饮水时,啮齿动物基因型饮用乙醇的意愿,能为酒精相对于其他基因型的强化价值提供合理的总体估计(格林和格雷厄姆,2008年)。然而,如上所述,偏好饮水研究可能永远无法避免味觉偏好的混杂作用,且通常产生的摄入量水平不足以产生具有药理学意义的血液酒精浓度。因此,人们仍在寻求更好的强化价值测量方法。在麦克林对本系列开创性综述中考虑的潜在动机因素中,我们可以有把握地得出结论,啮齿动物饮酒并非主要为了获取热量。味觉(和气味)的作用仍然是一个挑战。麦克林似乎是正确的,特别是那些避免饮酒的基因型可能是基于摄入前的感官线索这样做的;然而,摄入后的后果也很重要。坎宁安的胃内模型显示了摄入前和摄入后调节因素对最著名的例子,即通常几乎绝对避免饮酒的DBA/2J和HAP - 2小鼠的作用。随后的许多数据强化了麦克林早期的结论,即至少C57BL/6J小鼠不会通过调整摄入量来围绕给定的自我给药酒精剂量调节其摄入量。这让我们陷入了一个谜题,即为什么几乎所有基因型,即使是那些经过多代定向选择性培育以实现高自愿摄入量的基因型,也不会自我给药达到中毒剂量的酒精。自麦克林的综述以来,许多用于衡量酒精动机效应的巧妙试验被广泛使用,新的诱导依赖的方法已经取代了1968年普遍使用的旧方法。我试图找出遗传学力量可以有效发挥作用的有前景的领域,总体感觉我们现在对一些有待进行的重要实验有了更清晰的认识。

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本文引用的文献

1
Use of animal models of alcohol-related behavior.
Handb Clin Neurol. 2014;125:71-86. doi: 10.1016/B978-0-444-62619-6.00005-7.
3
Selection for drinking in the dark alters brain gene coexpression networks.
Alcohol Clin Exp Res. 2013 Aug;37(8):1295-303. doi: 10.1111/acer.12100. Epub 2013 Mar 29.
4
Behavioral neurobiology of alcohol addiction. Preface.
Curr Top Behav Neurosci. 2013;13:v-vii. doi: 10.1007/978-3-642-28720-6.
5
Compulsive drug use and its neural substrates.
Rev Neurosci. 2012;23(5-6):731-45. doi: 10.1515/revneuro-2012-0066.
6
Measurement of alcohol hangover severity: development of the Alcohol Hangover Severity Scale (AHSS).
Psychopharmacology (Berl). 2013 Feb;225(4):803-10. doi: 10.1007/s00213-012-2866-y. Epub 2012 Sep 25.
7
Time-dependent negative reinforcement of ethanol intake by alleviation of acute withdrawal.
Biol Psychiatry. 2013 Feb 1;73(3):249-55. doi: 10.1016/j.biopsych.2012.07.034. Epub 2012 Sep 18.
8
Context-induced relapse to alcohol seeking after punishment in a rat model.
Biol Psychiatry. 2013 Feb 1;73(3):256-62. doi: 10.1016/j.biopsych.2012.07.007. Epub 2012 Aug 9.
9
Animal models for medications development targeting alcohol abuse using selectively bred rat lines: neurobiological and pharmacological validity.
Pharmacol Biochem Behav. 2012 Nov;103(1):119-55. doi: 10.1016/j.pbb.2012.07.007. Epub 2012 Jul 25.
10
A promoter polymorphism in the Per3 gene is associated with alcohol and stress response.
Transl Psychiatry. 2012 Jan 31;2(1):e73. doi: 10.1038/tp.2011.71.

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