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Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses
It is widely accepted that the direction and magnitude of synaptic plasticity depends on post-synaptic calcium flux, where high levels of calcium lead to long-term potentiation and moderate levels lead to long-term depression. At synapses onto neurons in region CA1 of the hippocampus (and many other...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3899242/ https://www.ncbi.nlm.nih.gov/pubmed/24465987 http://dx.doi.org/10.1371/journal.pone.0086248 |
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author | Standage, Dominic Trappenberg, Thomas Blohm, Gunnar |
author_facet | Standage, Dominic Trappenberg, Thomas Blohm, Gunnar |
author_sort | Standage, Dominic |
collection | PubMed |
description | It is widely accepted that the direction and magnitude of synaptic plasticity depends on post-synaptic calcium flux, where high levels of calcium lead to long-term potentiation and moderate levels lead to long-term depression. At synapses onto neurons in region CA1 of the hippocampus (and many other synapses), NMDA receptors provide the relevant source of calcium. In this regard, post-synaptic calcium captures the coincidence of pre- and post-synaptic activity, due to the blockage of these receptors at low voltage. Previous studies show that under spike timing dependent plasticity (STDP) protocols, potentiation at CA1 synapses requires post-synaptic bursting and an inter-pairing frequency in the range of the hippocampal theta rhythm. We hypothesize that these requirements reflect the saturation of the mechanisms of calcium extrusion from the post-synaptic spine. We test this hypothesis with a minimal model of NMDA receptor-dependent plasticity, simulating slow extrusion with a calcium-dependent calcium time constant. In simulations of STDP experiments, the model accounts for latency-dependent depression with either post-synaptic bursting or theta-frequency pairing (or neither) and accounts for latency-dependent potentiation when both of these requirements are met. The model makes testable predictions for STDP experiments and our simple implementation is tractable at the network level, demonstrating associative learning in a biophysical network model with realistic synaptic dynamics. |
format | Online Article Text |
id | pubmed-3899242 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-38992422014-01-24 Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses Standage, Dominic Trappenberg, Thomas Blohm, Gunnar PLoS One Research Article It is widely accepted that the direction and magnitude of synaptic plasticity depends on post-synaptic calcium flux, where high levels of calcium lead to long-term potentiation and moderate levels lead to long-term depression. At synapses onto neurons in region CA1 of the hippocampus (and many other synapses), NMDA receptors provide the relevant source of calcium. In this regard, post-synaptic calcium captures the coincidence of pre- and post-synaptic activity, due to the blockage of these receptors at low voltage. Previous studies show that under spike timing dependent plasticity (STDP) protocols, potentiation at CA1 synapses requires post-synaptic bursting and an inter-pairing frequency in the range of the hippocampal theta rhythm. We hypothesize that these requirements reflect the saturation of the mechanisms of calcium extrusion from the post-synaptic spine. We test this hypothesis with a minimal model of NMDA receptor-dependent plasticity, simulating slow extrusion with a calcium-dependent calcium time constant. In simulations of STDP experiments, the model accounts for latency-dependent depression with either post-synaptic bursting or theta-frequency pairing (or neither) and accounts for latency-dependent potentiation when both of these requirements are met. The model makes testable predictions for STDP experiments and our simple implementation is tractable at the network level, demonstrating associative learning in a biophysical network model with realistic synaptic dynamics. Public Library of Science 2014-01-22 /pmc/articles/PMC3899242/ /pubmed/24465987 http://dx.doi.org/10.1371/journal.pone.0086248 Text en © 2014 Standage et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Standage, Dominic Trappenberg, Thomas Blohm, Gunnar Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses |
title | Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses |
title_full | Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses |
title_fullStr | Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses |
title_full_unstemmed | Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses |
title_short | Calcium-Dependent Calcium Decay Explains STDP in a Dynamic Model of Hippocampal Synapses |
title_sort | calcium-dependent calcium decay explains stdp in a dynamic model of hippocampal synapses |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3899242/ https://www.ncbi.nlm.nih.gov/pubmed/24465987 http://dx.doi.org/10.1371/journal.pone.0086248 |
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