Contet Candice
The Scripps Research Institute, Committee on the Neurobiology of Addictive Disorders, La Jolla, CA, USA.
Curr Psychopharmacol. 2012 Nov;1(4):301-314. doi: 10.2174/2211556011201040301.
Sensitivity to ethanol intoxication, propensity to drink ethanol and vulnerability to develop alcoholism are all influenced by genetic factors. Conversely, exposure to ethanol or subsequent withdrawal produce gene expression changes, which, in combination with environmental variables, may participate in the emergence of compulsive drinking and relapse. The present review offers an integrated perspective on brain gene expression profiling in rodent models of predisposition to differential ethanol sensitivity or consumption, in rats and mice subjected to acute or chronic ethanol exposure, as well as in human alcoholics. The functional categories over-represented among differentially expressed genes suggest that the transcriptional effects of chronic ethanol consumption contribute to the neuroplasticity and neurotoxicity characteristic of alcoholism. Importantly, ethanol produces distinct transcriptional changes within the different brain regions involved in intoxication, reinforcement and addiction. Special emphasis is put on recent profiling studies that have provided some insights into the molecular mechanisms potentially mediating genome-wide regulation of gene expression by ethanol. In particular, current evidence for a role of transcription factors, chromatin remodeling and microRNAs in coordinating the expression of large sets of genes in animals predisposed to excessive ethanol drinking or exposed to protracted abstinence, as well as in human alcoholics, is presented. Finally, studies that have compared ethanol with other drugs of abuse have highlighted common gene expression patterns that may play a central role in drug addiction. The availability of novel technologies and a focus on mechanistic approaches are shaping the future of ethanol transcriptomics.
对乙醇中毒的敏感性、饮酒倾向以及患酒精中毒的易感性均受遗传因素影响。相反,接触乙醇或随后戒酒会导致基因表达变化,这些变化与环境变量共同作用,可能促使强迫性饮酒和复饮的出现。本综述从综合角度阐述了在对乙醇敏感性或消耗量存在差异的啮齿动物模型、经历急性或慢性乙醇暴露的大鼠和小鼠以及人类酗酒者中进行脑基因表达谱分析的情况。差异表达基因中过度富集的功能类别表明,慢性乙醇摄入的转录效应促成了酒精中毒特有的神经可塑性和神经毒性。重要的是,乙醇在涉及中毒、强化和成瘾的不同脑区产生独特的转录变化。特别强调了近期的谱分析研究,这些研究为乙醇可能介导全基因组范围基因表达调控的分子机制提供了一些见解。具体而言,文中介绍了目前关于转录因子、染色质重塑和微小RNA在协调易患过度饮酒或经历长期戒酒的动物以及人类酗酒者中大量基因表达方面作用的证据。最后,将乙醇与其他滥用药物进行比较的研究突出了可能在药物成瘾中起核心作用的共同基因表达模式。新技术的出现以及对机制性方法的关注正在塑造乙醇转录组学的未来。