Costa-Mattioli Mauro, Sonenberg Nahum
Department of Biochemistry and McGill Cancer Center, 3655 Promendde Sir William Osler, McGill University, Montréal, QC H3G 1Y6, Canada.
Prog Brain Res. 2008;169:81-95. doi: 10.1016/S0079-6123(07)00005-2.
A critical requirement for the conversion of the labile short-term memory (STM) into the consolidated long-term memory (LTM) is new gene expression (new mRNAs and protein synthesis). The first clues to the molecular mechanisms of the switch from short-term to LTM emerged from studies on protein synthesis in different species. Initially, it was shown that LTM can be distinguished from STM by its susceptibility to protein synthesis inhibitors. Later, it was found that long-lasting synaptic changes, which are believed to be a key cellular mechanism by which information is stored, are also dependent on new protein synthesis. Although the role of protein synthesis in memory was reported more than 40 years ago, recent molecular, genetic, and biochemical studies have provided fresh insights into the molecular mechanisms underlying these processes. In this chapter, we provide an overview of the role of translational control by the eIF2alpha signaling pathway in long-term synaptic plasticity and memory consolidation.
将不稳定的短期记忆（STM）转化为巩固的长期记忆（LTM）的一个关键要求是新基因表达（新的mRNA和蛋白质合成）。关于从短期记忆向长期记忆转变的分子机制的最初线索来自对不同物种蛋白质合成的研究。最初，研究表明长期记忆可因其对蛋白质合成抑制剂的敏感性而与短期记忆区分开来。后来发现，持久的突触变化被认为是信息存储的关键细胞机制，它也依赖于新的蛋白质合成。尽管蛋白质合成在记忆中的作用在40多年前就已被报道，但最近的分子、遗传和生化研究为这些过程背后的分子机制提供了新的见解。在本章中，我们概述了eIF2α信号通路的翻译控制在长期突触可塑性和记忆巩固中的作用。
