Making synaptic plasticity and memory last: mechanisms of translational regulation

被引:282
作者
Richter, Joel D. [1 ]
Klann, Eric [2 ]
机构
[1] Univ Massachusetts, Program Mol Med, Sch Med, Worcester, MA 01605 USA
[2] NYU, Ctr Neural Sci, New York, NY 10003 USA
关键词
Translation; neuron; synaptic plasticity; memory; MENTAL-RETARDATION PROTEIN; FRAGILE-X-SYNDROME; LONG-TERM DEPRESSION; RECEPTOR-DEPENDENT TRANSLATION; CAMKII MESSENGER-RNA; INITIATION-FACTOR; 4E; ELONGATION-FACTOR; 1A; MAMMALIAN TARGET; MOUSE MODEL; SYNTHESIS INHIBITION;
D O I
10.1101/gad.1735809
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Synaptic transmission in neurons is a measure of communication at synapses, the points of contact between axons and dendrites. The magnitude of synaptic transmission is a reflection of the strength of these synaptic connections, which in turn can be altered by the frequency with which the synapses are stimulated, the arrival of stimuli from other neurons in the appropriate temporal window, and by neurotrophic factors and neuromodulators. The ability of synapses to undergo lasting biochemical and morphological changes in response to these types of stimuli and neuromodulators is known as synaptic plasticity, which likely forms the cellular basis for learning and memory, although the relationship between any one form synaptic plasticity and a particular type of memory is unclear. RNA metabolism, particularly translational control at or near the synapse, is one process that controls long-lasting synaptic plasticity and, by extension, several types of memory formation and consolidation. Here, we review recent studies that reflect the importance and challenges of investigating the role of mRNA translation in synaptic plasticity and memory formation.
引用
收藏
页码:1 / 11
页数:11
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