Transcriptional and epigenetic regulation of microglia in substance use disorders

IF 2.6 3区医学 Q3 NEUROSCIENCES Molecular and Cellular Neuroscience Pub Date : 2023-06-01 DOI:10.1016/j.mcn.2023.103838

Samara J. Vilca , Alexander V. Margetts , Tate A. Pollock , Luis M. Tuesta

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引用次数: 3

Abstract

Microglia are widely known for their role in immune surveillance and for their ability to refine neurocircuitry during development, but a growing body of evidence suggests that microglia may also play a complementary role to neurons in regulating the behavioral aspects of substance use disorders. While many of these efforts have focused on changes in microglial gene expression associated with drug-taking, epigenetic regulation of these changes has yet to be fully understood. This review provides recent evidence supporting the role of microglia in various aspects of substance use disorder, with particular focus on changes to the microglial transcriptome and the potential epigenetic mechanisms driving these changes. Further, this review discusses the latest technical advances in low-input chromatin profiling and highlights the current challenges for studying these novel molecular mechanisms in microglia.

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物质使用障碍中小胶质细胞的转录和表观遗传调控

小胶质细胞因其在免疫监测中的作用以及在发育过程中改善神经回路的能力而广为人知，但越来越多的证据表明，小胶质细胞在调节物质使用障碍的行为方面也可能与神经元发挥互补作用。虽然这些努力中的许多都集中在与服药相关的小胶质细胞基因表达的变化上，但这些变化的表观遗传学调控尚待充分理解。这篇综述提供了支持小胶质细胞在物质使用障碍的各个方面的作用的最新证据，特别关注小胶质细胞转录组的变化以及驱动这些变化的潜在表观遗传学机制。此外，这篇综述讨论了低输入染色质图谱的最新技术进展，并强调了研究小胶质细胞中这些新分子机制的当前挑战。

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来源期刊

Molecular and Cellular Neuroscience 医学-神经科学

CiteScore

5.60

自引率

0.00%

发文量

审稿时长

37 days

期刊介绍： Molecular and Cellular Neuroscience publishes original research of high significance covering all aspects of neurosciences indicated by the broadest interpretation of the journal''s title. In particular, the journal focuses on synaptic maintenance, de- and re-organization, neuron-glia communication, and de-/regenerative neurobiology. In addition, studies using animal models of disease with translational prospects and experimental approaches with backward validation of disease signatures from human patients are welcome.