Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity

Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity

Neuronal activity-dependent synaptic plasticity, a basis for learning and memory, is tightly correlated with the pattern of increase in intracellular Ca2+ concentration ([Ca2+]i). Here, using combined application of electrophysiological experiments and systems biological simulation, we show that suc...

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Main Authors: Kawaguchi, Shin-ya, Nagasaki, Nobuhiro, Hirano, Tomoo
Format: Online
Language:English
Published: Nature Publishing Group 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216624/
id pubmed-3216624
recordtype oai_dc
spelling pubmed-32166242011-12-22 Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity Kawaguchi, Shin-ya Nagasaki, Nobuhiro Hirano, Tomoo Article Neuronal activity-dependent synaptic plasticity, a basis for learning and memory, is tightly correlated with the pattern of increase in intracellular Ca2+ concentration ([Ca2+]i). Here, using combined application of electrophysiological experiments and systems biological simulation, we show that such a correlation dynamically changes depending on the context of [Ca2+]i increase. In a cerebellar Purkinje cell, long-term potentiation of inhibitory GABAA receptor responsiveness (called rebound potentiation; RP) was induced by [Ca2+]i increase in a temporally integrative manner through sustained activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII). However, the RP establishment was canceled by coupling of two patterns of RP-inducing [Ca2+]i increase depending on the temporal sequence. Negative feedback signaling by phospho-Thr305/306 CaMKII detected the [Ca2+]i context, and assisted the feedforward inhibition of CaMKII through PDE1, resulting in the RP impairment. The [Ca2+]i context-dependent dynamic regulation of synaptic plasticity might contribute to the temporal refinement of information flow in neuronal networks. Nature Publishing Group 2011-11-04 /pmc/articles/PMC3216624/ /pubmed/22355660 http://dx.doi.org/10.1038/srep00143 Text en Copyright © 2011, Macmillan Publishers Limited. All rights reserved http://creativecommons.org/licenses/by-nc-sa/3.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-ShareALike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Kawaguchi, Shin-ya
Nagasaki, Nobuhiro
Hirano, Tomoo
spellingShingle Kawaguchi, Shin-ya
Nagasaki, Nobuhiro
Hirano, Tomoo
Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity
author_facet Kawaguchi, Shin-ya
Nagasaki, Nobuhiro
Hirano, Tomoo
author_sort Kawaguchi, Shin-ya
title Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity
title_short Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity
title_full Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity
title_fullStr Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity
title_full_unstemmed Dynamic impact of temporal context of Ca2+ signals on inhibitory synaptic plasticity
title_sort dynamic impact of temporal context of ca2+ signals on inhibitory synaptic plasticity
description Neuronal activity-dependent synaptic plasticity, a basis for learning and memory, is tightly correlated with the pattern of increase in intracellular Ca2+ concentration ([Ca2+]i). Here, using combined application of electrophysiological experiments and systems biological simulation, we show that such a correlation dynamically changes depending on the context of [Ca2+]i increase. In a cerebellar Purkinje cell, long-term potentiation of inhibitory GABAA receptor responsiveness (called rebound potentiation; RP) was induced by [Ca2+]i increase in a temporally integrative manner through sustained activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII). However, the RP establishment was canceled by coupling of two patterns of RP-inducing [Ca2+]i increase depending on the temporal sequence. Negative feedback signaling by phospho-Thr305/306 CaMKII detected the [Ca2+]i context, and assisted the feedforward inhibition of CaMKII through PDE1, resulting in the RP impairment. The [Ca2+]i context-dependent dynamic regulation of synaptic plasticity might contribute to the temporal refinement of information flow in neuronal networks.
publisher Nature Publishing Group
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216624/
_version_ 1611487920339812352

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