Abstract
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.
Original language | English |
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Article number | 20130141 |
Number of pages | 9 |
Journal | Philosophical Transactions of the Royal Society B: Biological Sciences |
Volume | 369 |
Issue number | 1633 |
DOIs | |
Publication status | Published - 5 Jan 2014 |
Keywords / Materials (for Non-textual outputs)
- long-term potentiation
- decay
- homeostatic scaling
- metaplasticity
- forgetting
- KINASE M-ZETA
- HIPPOCAMPAL SYNAPTIC PLASTICITY
- PKM-ZETA
- NMDA RECEPTORS
- SPATIAL MEMORY
- VISUAL-CORTEX
- TYROSINE PHOSPHORYLATION
- PROTEIN-SYNTHESIS
- SUBUNIT GLUR2
- FEAR MEMORY