致病记忆的神经表观遗传调控

Stephanie E. Sillivan , Thomas Vaissière , Courtney A. Miller
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引用次数: 25

摘要

我们独特的记忆决定了我们的个性,塑造了我们未来与世界的互动。记忆的神经生物学基础的显著进展已经确定了支持记忆稳定性的关键表观遗传机制。在DNA甲基化、组蛋白修饰和非编码rna水平上的各种形式的表观遗传调控可以调节记忆过程所需的转录和翻译事件。通过改变大脑的情感、奖励和记忆回路中的细胞结构,这些表观遗传修饰也与持久的、致病的记忆有关。在这篇综述中,我们将通过关注两种由异常记忆关联引起的神经精神疾病:物质使用障碍和创伤后应激障碍,来深入研究表观遗传失调与致病性记忆机制的相关性。随着我们认识的提高,神经表观遗传机制可能有一天会被用来开发治疗这些慢性复发性疾病的新治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuroepigenetic regulation of pathogenic memories

Our unique collection of memories determines our individuality and shapes our future interactions with the world. Remarkable advances into the neurobiological basis of memory have identified key epigenetic mechanisms that support the stability of memory. Various forms of epigenetic regulation at the levels of DNA methylation, histone modification, and noncoding RNAs can modulate transcriptional and translational events required for memory processes. By changing the cellular profile in the brain’s emotional, reward, and memory circuits, these epigenetic modifications have also been linked to perseverant, pathogenic memories. In this review, we will delve into the relevance of epigenetic dysregulation to pathogenic memory mechanisms by focusing on 2 neuropsychiatric disorders perpetuated by aberrant memory associations: substance use disorder and post-traumatic stress disorder. As our understanding improves, neuroepigenetic mechanisms may someday be harnessed to develop novel therapeutic targets for the treatment of these chronic, relapsing disorders.

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