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
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
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DOI：
10.1098/rstb.2013.0141
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发表时间：
2014-01-05
影响因子：
6.3
通讯作者：
Wang, Yu-Tian
中科院分区：
文献类型：
--
作者：
Hardt, Oliver;Nader, Karim;Wang, Yu-Tian
参与建立长时程增强（LTP）的分子过程已被很好地表征，但对早期和晚期LTP（E-LTP和L-LTP）的衰减知之甚少。我们回顾了最近的进展，在描述参与维持LTP和稳态可塑性的机制。我们讨论了这些现象如何与可能支持突触增强随时间推移而丧失的过程有关，以及它们如何有助于短期和长期记忆的遗忘。我们建议，稳态降尺度介导的损失E-LTP，化生参数确定衰减率的L-LTP，而这两个过程需要的活动依赖性的清除突触后的GluA 2-AMPA受体。
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.