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...

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Bibliographic Details
Published in:eLife 2021-12, Vol.10
Main Authors: Tao, Wucheng, Lee, Joel, Chen, Xiumin, Díaz-Alonso, Javier, Zhou, Jing, Pleasure, Samuel, Nicoll, Roger A
Format: Article
Language:English
Subjects:
Analysis
Animals
Ca2+/calmodulin-dependent protein kinase II
Calcium-binding protein
Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics
Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism
Calmodulin
camk2
CRISPR
hippocampus
Information storage
ion channel
Learning
Long-Term Potentiation
LTP
Memory
Mice
Neurons
Neuroscience
Peptides
Pharmaceutical industry
Physiology
receptor
synapse
Synaptic Transmission
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Summary: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 -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.
ISSN:2050-084X
2050-084X
DOI:10.7554/elife.60360