Synaptic memory requires CaMKII

Long-term potentiation (LTP) is arguably the most compelling cellular model for learning and memory. While the mechanisms underlying the induction of LTP (‘learning’) are well understood, the maintenance of LTP (‘memory’) has remained contentious over the last 20 years. Here, we find that Ca(2+)-cal...

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Detalles Bibliográficos
Autores principales: Tao, Wucheng, Lee, Joel, Chen, Xiumin, Díaz-Alonso, Javier, Zhou, Jing, Pleasure, Samuel, Nicoll, Roger A
Formato: Online Artículo Texto
Lenguaje:English
Publicado: eLife Sciences Publications, Ltd 2021
Materias:
Neuroscience
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798046/
https://www.ncbi.nlm.nih.gov/pubmed/34908526
http://dx.doi.org/10.7554/eLife.60360
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author Tao, Wucheng
Lee, Joel
Chen, Xiumin
Díaz-Alonso, Javier
Zhou, Jing
Pleasure, Samuel
Nicoll, Roger A
author_facet Tao, Wucheng
Lee, Joel
Chen, Xiumin
Díaz-Alonso, Javier
Zhou, Jing
Pleasure, Samuel
Nicoll, Roger A
author_sort Tao, Wucheng
collection PubMed
description Long-term potentiation (LTP) is arguably the most compelling cellular model for learning and memory. While the mechanisms underlying the induction of LTP (‘learning’) are well understood, the maintenance of LTP (‘memory’) has remained contentious over the last 20 years. Here, we find that Ca(2+)-calmodulin-dependent kinase II (CaMKII) contributes to synaptic transmission and is required LTP maintenance. Acute inhibition of CaMKII erases LTP and transient inhibition of CaMKII enhances subsequent LTP. These findings strongly support the role of CaMKII as a molecular storage device.
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spelling pubmed-87980462022-01-31 Synaptic memory requires CaMKII Tao, Wucheng Lee, Joel Chen, Xiumin Díaz-Alonso, Javier Zhou, Jing Pleasure, Samuel Nicoll, Roger A eLife Neuroscience Long-term potentiation (LTP) is arguably the most compelling cellular model for learning and memory. While the mechanisms underlying the induction of LTP (‘learning’) are well understood, the maintenance of LTP (‘memory’) has remained contentious over the last 20 years. Here, we find that Ca(2+)-calmodulin-dependent kinase II (CaMKII) contributes to synaptic transmission and is required LTP maintenance. Acute inhibition of CaMKII erases LTP and transient inhibition of CaMKII enhances subsequent LTP. These findings strongly support the role of CaMKII as a molecular storage device. eLife Sciences Publications, Ltd 2021-12-15 /pmc/articles/PMC8798046/ /pubmed/34908526 http://dx.doi.org/10.7554/eLife.60360 Text en © 2021, Tao et al https://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Neuroscience
Tao, Wucheng
Lee, Joel
Chen, Xiumin
Díaz-Alonso, Javier
Zhou, Jing
Pleasure, Samuel
Nicoll, Roger A
Synaptic memory requires CaMKII
title Synaptic memory requires CaMKII
title_full Synaptic memory requires CaMKII
title_fullStr Synaptic memory requires CaMKII
title_full_unstemmed Synaptic memory requires CaMKII
title_short Synaptic memory requires CaMKII
title_sort synaptic memory requires camkii
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798046/
https://www.ncbi.nlm.nih.gov/pubmed/34908526
http://dx.doi.org/10.7554/eLife.60360
work_keys_str_mv AT taowucheng synapticmemoryrequirescamkii
AT leejoel synapticmemoryrequirescamkii
AT chenxiumin synapticmemoryrequirescamkii
AT diazalonsojavier synapticmemoryrequirescamkii
AT zhoujing synapticmemoryrequirescamkii
AT pleasuresamuel synapticmemoryrequirescamkii
AT nicollrogera synapticmemoryrequirescamkii

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