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Synaptic memory requires CaMKII.

eLife (2021-12-16)
Wucheng Tao, Joel Lee, Xiumin Chen, Javier Díaz-Alonso, Jing Zhou, Samuel Pleasure, Roger A Nicoll
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 Ca2+-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.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Calmodulin Kinase IINtide, Myristoylated, The myristoylated form of CaMK IINtide.
Sigma-Aldrich
Autocamtide-2 Related Inhibitory Peptide, Myristoylated, The Autocamtide-2 Related Inhibitory Peptide, Myristoylated controls the biological activity of calmodulin-dependent protein kinase II. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.