GluA2-dependent AMPA receptor endocytosis and the decay of early and late long-term potentiation: possible mechanisms for forgetting of short- and long-term memories

被引:63
作者
Hardt, Oliver [1 ]
Nader, Karim [2 ]
Wang, Yu-Tian [3 ]
机构
[1] Univ Edinburgh, Ctr Cognit & Neural Syst, Edinburgh, Midlothian, Scotland
[2] McGill Univ, Dept Psychol, Montreal, PQ, Canada
[3] Univ British Columbia, Brain Res Ctr, Vancouver, BC V5Z 1M9, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
long-term potentiation; decay; homeostatic scaling; metaplasticity; forgetting; KINASE M-ZETA; HIPPOCAMPAL SYNAPTIC PLASTICITY; PKM-ZETA; TYROSINE PHOSPHORYLATION; NMDA RECEPTORS; SPATIAL MEMORY; SUBUNIT GLUR2; LATE-PHASE; DEPRESSION; LTP;
D O I
10.1098/rstb.2013.0141
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The molecular processes involved in establishing long-term potentiation (LTP) have been characterized well, but the decay of early and late LTP (E-LTP and L-LTP) is poorly understood. We review recent advances in describing the mechanisms involved in maintaining LTP and homeostatic plasticity. We discuss how these phenomena could relate to processes that might underpin the loss of synaptic potentiation over time, and how they might contribute to the forgetting of short-term and long-term memories. We propose that homeostatic downscaling mediates the loss of E-LTP, and that metaplastic parameters determine the decay rate of L-LTP, while both processes require the activity-dependent removal of postsynaptic GluA2-containing AMPA receptors.
引用
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页数:9
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