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      Translational regulatory mechanisms in synaptic plasticity and memory storage.

      Progress in molecular biology and translational science
      Animals, Disease, genetics, Eukaryotic Initiation Factor-2, metabolism, Humans, Memory, physiology, Neuronal Plasticity, Protein Biosynthesis, Signal Transduction, Synapses

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          Abstract

          Synaptic activity-dependent protein synthesis is required to convert a labile short-term memory (STM) into a persistent long-term memory (LTM). Indeed, genetic or pharmacological inhibition of translation impairs LTM, but not STM. Long-lasting biochemical and morphological changes of synapses, which underlie learning and memory, also require new protein synthesis. In recent years, a large number of experiments have yielded much new information about the processes that govern translational control of synaptic plasticity during learning and memory processes. Signaling pathways that modulate mRNA translation play critical roles in these processes. In this chapter, we review the mechanisms by which certain translational regulators including eIF2alpha, 4E-BP, S6K, and CPEB control long-term synaptic plasticity and memory consolidation and their involvement in neurologic disease. Copyright © 2009 Elsevier Inc. All rights reserved.

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          Author and article information

          Journal
          20374745
          10.1016/S1877-1173(09)90008-4

          Chemistry
          Animals,Disease,genetics,Eukaryotic Initiation Factor-2,metabolism,Humans,Memory,physiology,Neuronal Plasticity,Protein Biosynthesis,Signal Transduction,Synapses

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