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
Author(s) -
Oliver Hardt,
Karim Nader,
Yu Tian Wang
Publication year - 2013
Publication title -
philosophical transactions of the royal society b biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.753
H-Index - 272
eISSN - 1471-2970
pISSN - 0962-8436
DOI - 10.1098/rstb.2013.0141
Subject(s) - long term potentiation , ampa receptor , neuroscience , forgetting , metaplasticity , postsynaptic potential , synaptic plasticity , homeostatic plasticity , long term depression , biology , synaptic scaling , nmda receptor , receptor , psychology , cognitive psychology , biochemistry
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.
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