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组蛋白乙酰化在记忆巩固过程中被招募,作为更强记忆的分子特征。

Histone acetylation is recruited in consolidation as a molecular feature of stronger memories.

作者信息

Federman Noel, Fustiñana Maria Sol, Romano Arturo

机构信息

Laboratorio de Neurobiología de la Memoria, Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, IFIByNE (UBA CONICET), Ciudad Universitaria,1428EHA Buenos Aires, Argentina.

出版信息

Learn Mem. 2009 Sep 30;16(10):600-6. doi: 10.1101/lm.1537009. Print 2009 Oct.

DOI:10.1101/lm.1537009
PMID:19794185
Abstract

Gene expression is a key process for memory consolidation. Recently, the participation of epigenetic mechanisms like histone acetylation was evidenced in long-term memories. However, until now the training strength required and the persistence of the chromatin acetylation recruited are not well characterized. Here we studied whether histone acetylation is involved in consolidation in invertebrates, whether it depends on the training strength, and whether it is a permanent or transient mechanism. We used a well-characterized memory model in invertebrates, the context-signal memory in crabs. Our results show no changes in histone 3 (H3) acetylation during consolidation of a standard training protocol. However, strong training induced a significant increase in H3 acetylation 1-h post-training, returning to basal levels afterward. Accordingly, the administration of histone deacetylase inhibitors sodium butyrate (NaB) and trichostatin A allowed a weak training to induce long-term memory. NaB enhanced memory in two phases during consolidation. These findings support that H3 acetylation (1) is involved in consolidation, (2) occurs only after strong training, (3) is a transient process, and (4) memory is enhanced in two phases. The coincidence of these phases with other mechanisms of gene expression is discussed.

摘要

基因表达是记忆巩固的关键过程。最近,组蛋白乙酰化等表观遗传机制在长期记忆中的参与得到了证实。然而,到目前为止,所需的训练强度以及所募集的染色质乙酰化的持续性尚未得到很好的表征。在这里,我们研究了组蛋白乙酰化是否参与无脊椎动物的记忆巩固,它是否依赖于训练强度,以及它是一种永久性还是短暂性机制。我们使用了一种在无脊椎动物中特征明确的记忆模型,即螃蟹的情境信号记忆。我们的结果表明,在标准训练方案的巩固过程中,组蛋白3(H3)乙酰化没有变化。然而,高强度训练在训练后1小时诱导H3乙酰化显著增加,随后恢复到基础水平。相应地,给予组蛋白去乙酰化酶抑制剂丁酸钠(NaB)和曲古抑菌素A可使弱训练诱导长期记忆。NaB在巩固过程的两个阶段增强了记忆。这些发现支持H3乙酰化(1)参与巩固,(2)仅在高强度训练后发生,(3)是一个短暂的过程,以及(4)记忆在两个阶段得到增强。我们还讨论了这些阶段与其他基因表达机制的一致性。

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