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酒精 binge drinking 的临床前研究。

Preclinical studies of alcohol binge drinking.

机构信息

Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University and VA Medical Center, Portland, Oregon 97239, USA.

出版信息

Ann N Y Acad Sci. 2011 Jan;1216:24-40. doi: 10.1111/j.1749-6632.2010.05895.x.

DOI:10.1111/j.1749-6632.2010.05895.x
PMID:21272009
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3076900/
Abstract

Binge drinking is prevalent and has serious biomedical consequences. In children, adolescents, and young adults, it is a prominent risk factor for later development of alcohol-use disorders. Many preclinical models have been employed to study the genetic risks for and biomedical consequences of alcohol drinking. However, these models historically did not result in blood-alcohol concentrations (BACs) exceeding 80 mg%; this relatively modest level is the threshold that currently defines a binge session, according to the NIAAA and CDC. Nevertheless, in alcohol-dependent rodents, binge drinking has been well documented. Key neurobiological substrates localized to brain reward and stress systems have been identified. Studies of newer models of binge drinking without dependence are reviewed here. In these models, rodents, non-human primates, and flies will drink enough to reach high BACs. They often display observable signs of intoxication. The neurobiological consequences of these episodes of binge drinking without dependence are reviewed, and preliminary evidence for roles for GABA, glutamate, opioid peptides, and corticotropin releasing factor are discussed, as is the need for more work to identify the antecedents and consequences of binge drinking in both animal models and humans.

摘要

binge drinking (狂饮)很常见,且会带来严重的生物医学后果。在儿童、青少年和年轻人中,它是日后发展为酒精使用障碍的一个主要风险因素。许多临床前模型被用于研究饮酒的遗传风险和生物医学后果。然而,这些模型在历史上并未导致血液酒精浓度(BAC)超过 80mg%;根据 NIAAA 和 CDC 的定义,这一相对适中的水平是目前界定狂饮期的阈值。尽管如此,在酒精依赖的啮齿动物中,狂饮行为已得到充分证实。已确定了定位于大脑奖励和应激系统的关键神经生物学基质。本文综述了无依赖的新型狂饮模型研究。在这些模型中,啮齿动物、非人类灵长类动物和苍蝇会喝到足以达到高 BAC 的量。它们经常表现出明显的醉酒迹象。本文综述了这些无依赖狂饮发作的神经生物学后果,并讨论了 GABA、谷氨酸、阿片肽和促肾上腺皮质释放因子的作用初步证据,还讨论了在动物模型和人类中识别狂饮的前提和后果的必要性。

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