Translational regulatory mechanisms in synaptic plasticity and memory storage.
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.
Costa-Mattioli
Mauro
M
Department of Neuroscience, Learning & Memory Center, Baylor College of Medicine, Houston, Texas 77030, USA.
Sonenberg
Nahum
N
Richter
Joel D
JD
D000818:Animals; D004194:Disease / Q000235:genetics; D015852:Eukaryotic Initiation Factor-2 / Q000378:metabolism; D006801:Humans; D008568:Memory / Q000502:physiology*; D009473:Neuronal Plasticity / Q000235:genetics*; D014176:Protein Biosynthesis / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics; D013569:Synapses / Q000235:genetics*
D015852:Eukaryotic Initiation Factor-2