Does stress remove the HDAC brakes for the formation and persistence of long-term memory?
Does stress remove the HDAC brakes for the formation and persistence of long-term memory?
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DOI：
10.1016/j.nlm.2013.10.007
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发表时间：
2014-07
影响因子：
2.7
通讯作者：
Wood, Marcelo A.
中科院分区：
文献类型：
--
作者：
White, Andre O.;Wood, Marcelo A.
关键词：
几十年来，人们已经知道基因表达是持久记忆形式所必需的。在过去的十年中，对记忆过程中表观遗传机制的研究揭示了基因表达调控的另一层复杂性。表观遗传机制不仅提供了蛋白质调控复合物的复杂性，这些蛋白质调控复合物控制特定细胞功能的协调转录，而且表观基因组编码了整合特定细胞功能的经验和细胞历史的关键信息。因此，表观遗传机制为记忆过程提供了一种独特的基因表达调控机制。这可能就是为什么基因表达的关键负调控因子，如组蛋白脱乙酰酶（HDAC），对记忆的形成和持久性有强大的影响。例如，HDAC抑制已被证明可以将阈下学习事件转化为强大的长期记忆，并且还产生一种形式的长期记忆，该长期记忆持续超过正常长期记忆失败的点。从学习和记忆的角度来看，本文探讨的一个关键问题是，压力依赖性信号是否通过HDAC依赖性机制驱动长期记忆的形成和持续。
It has been known for numerous decades that gene expression is required for long-lasting forms of memory. In the past decade, the study of epigenetic mechanisms in memory processes has revealed yet another layer of complexity in the regulation of gene expression. Epigenetic mechanisms do not only provide complexity in the protein regulatory complexes that control coordinate transcription for specific cell function, but the epigenome encodes critical information that integrates experience and cellular history for specific cell functions as well. Thus, epigenetic mechanisms provide a unique mechanism of gene expression regulation for memory processes. This may be why critical negative regulators of gene expression, such as histone deacetylases (HDACs), have powerful effects on the formation and persistence of memory. For example, HDAC inhibition has been shown to transform a subthreshold learning event into robust long-term memory and also generate a form of long-term memory that persists beyond the point at which normal long-term memory fails. A key question that is explored in this review, from a learning and memory perspective, is whether stress-dependent signaling drives the formation and persistence of long-term memory via HDAC-dependent mechanisms.
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影响因子：
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