Synaptic memory requires CaMKII.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 34908526.
- Also identified by DOI 10.7554/eLife.60360 and PMC identifier 8798046.
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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 Ca<sup>2+</sup>-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.
Medical subject headings
- Calcium-Calmodulin-Dependent Protein Kinase Type 2
- Long-Term Potentiation
- Synaptic Transmission