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.
All data generated or analysed during this study are included in the manuscript and supporting files.
No external funding was received for this work.
Animal experimentation: All the experimental procedures on animals were approved by the UCSF Animal Care and Use Committee, BUA # BU002466-04C
- Nils Brose, Max Planck Institute of Experimental Medicine, Germany
- Received: June 24, 2020
- Accepted: December 14, 2021
- Accepted Manuscript published: December 15, 2021 (version 1)
© 2021, Tao et al.
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