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...

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Autores principales:	Dominic Standage, Thomas Trappenberg, Gunnar Blohm
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7be001265de94d1ab95e99aba2909c00
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spelling	oai:doaj.org-article:7be001265de94d1ab95e99aba2909c002021-11-18T08:36:28ZCalcium-dependent calcium decay explains STDP in a dynamic model of hippocampal synapses.1932-620310.1371/journal.pone.0086248https://doaj.org/article/7be001265de94d1ab95e99aba2909c002014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24465987/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203It 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.Dominic StandageThomas TrappenbergGunnar BlohmPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 1, p e86248 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Dominic Standage Thomas Trappenberg Gunnar Blohm Calcium-dependent calcium decay explains STDP in a dynamic model of hippocampal synapses.
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	article
author	Dominic Standage Thomas Trappenberg Gunnar Blohm
author_facet	Dominic Standage Thomas Trappenberg Gunnar Blohm
author_sort	Dominic Standage
title	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_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_sort	calcium-dependent calcium decay explains stdp in a dynamic model of hippocampal synapses.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/7be001265de94d1ab95e99aba2909c00
work_keys_str_mv	AT dominicstandage calciumdependentcalciumdecayexplainsstdpinadynamicmodelofhippocampalsynapses AT thomastrappenberg calciumdependentcalciumdecayexplainsstdpinadynamicmodelofhippocampalsynapses AT gunnarblohm calciumdependentcalciumdecayexplainsstdpinadynamicmodelofhippocampalsynapses
_version_	1718421571074260992

Calcium-dependent calcium decay explains STDP in a dynamic model of hippocampal synapses.

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