RESEARCH ARTICLE Synaptic memory requires CaMKII
RESEARCH ARTICLE Synaptic memory requires CaMKII
Abstract Long-term potentiation is arguably the most compelling cellular model for learning and memory. While the mechanisms underlying the induction of long-term potentiation, or learning, are well understood, the maintenance of long-term potentiation, or memory, has remained contentious over the last twenty years. Here, we find that calcium-calmodulin-dependent kinase II contributes to synaptic transmission and is required for long-term potentiation maintenance. Acute inhibition of calcium-calmodulin-dependent kinase II erases long-term potentiation and transient inhibition of calcium-calmodulin-dependent kinase II enhances subsequent long-term potentiation. These findings strongly support the role of calcium-calmodulin-dependent kinase II as a molecular storage device.
Editor's evaluation
Editor's evaluation
The article addresses the decades-old unresolved question as to whether calcium-calmodulin-dependent kinase II is required for the maintenance of synaptic long-term potentiation, and shows, based on a set of elegant experiments, that it indeed is.