Synaptic memory requires CaMKII
Abstract
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 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 devise.
Data availability
All data generated or analysed during this study are included in the manuscript and supporting files.
Article and author information
Author details
Funding
No external funding was received for this work.
Reviewing Editor
- Nils Brose, Max Planck Institute of Experimental Medicine, Germany
Ethics
Animal experimentation: All the experimental procedures on animals were approved by the UCSF Animal Care and Use Committee, BUA # BU002466-04C
Version history
- Received: June 24, 2020
- Accepted: December 14, 2021
- Accepted Manuscript published: December 15, 2021 (version 1)
- Version of Record published: January 28, 2022 (version 2)
Copyright
© 2021, Tao et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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