Nash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
Nash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
Biol Psychiatry. 2020 Jan 1;87(1):22-33. doi: 10.1016/j.biopsych.2019.06.027. Epub 2019 Jul 8.
Opioid use kills tens of thousands of Americans each year, devastates families and entire communities, and cripples the health care system. Exposure to opioids causes long-term changes to brain regions involved in reward processing and motivation, leading vulnerable individuals to engage in pathological drug seeking and drug taking that can remain a lifelong struggle. The persistence of these neuroadaptations is mediated in part by epigenetic remodeling of gene expression programs in discrete brain regions. Although the majority of work examining how epigenetic modifications contribute to addiction has focused on psychostimulants such as cocaine, research into opioid-induced changes to the epigenetic landscape is emerging. This review summarizes our knowledge of opioid-induced epigenetic modifications and their consequential changes to gene expression. Current evidence points toward opioids promoting higher levels of permissive histone acetylation and lower levels of repressive histone methylation as well as alterations to DNA methylation patterns and noncoding RNA expression throughout the brain's reward circuitry. Additionally, studies manipulating epigenetic enzymes in specific brain regions are beginning to build causal links between these epigenetic modifications and changes in addiction-related behavior. Moving forward, studies must leverage advanced chromatin analysis and next-generation sequencing approaches combined with bioinformatics pipelines to identify novel gene networks regulated by particular epigenetic modifications. Improved translational relevance also requires increased focus on volitional drug-intake models and standardization of opioid exposure paradigms. Such work will significantly advance our understanding of how opioids cause persistent changes to brain function and will provide a platform on which to develop interventions for treating opioid addiction.
阿片类药物的使用每年导致成千上万的美国人死亡,摧毁了家庭和整个社区,并使医疗保健系统瘫痪。阿片类药物的暴露会导致参与奖励处理和动机的大脑区域发生长期变化,使易受伤害的个体参与病理性药物寻求和药物滥用,这可能成为一生的斗争。这些神经适应的持续存在部分是由离散大脑区域中基因表达程序的表观遗传重塑介导的。尽管大多数研究探索了表观遗传修饰如何导致成瘾的工作都集中在可卡因等精神兴奋剂上,但对阿片类药物引起的表观遗传景观变化的研究正在出现。这篇综述总结了我们对阿片类药物引起的表观遗传修饰及其对基因表达的 consequential 变化的认识。目前的证据表明,阿片类药物促进了更高水平的允许性组蛋白乙酰化和更低水平的抑制性组蛋白甲基化,以及整个大脑奖励回路中 DNA 甲基化模式和非编码 RNA 表达的改变。此外,在特定脑区操纵表观遗传酶的研究开始在这些表观遗传修饰和与成瘾相关的行为变化之间建立因果关系。展望未来,研究必须利用先进的染色质分析和下一代测序方法结合生物信息学管道来识别受特定表观遗传修饰调节的新基因网络。提高转化相关性还需要更加关注自愿药物摄入模型和阿片类药物暴露范式的标准化。这项工作将极大地提高我们对阿片类药物如何导致大脑功能持久变化的理解,并为治疗阿片类药物成瘾提供一个干预平台。