alphaCaMKII autophosphorylation: a fast track to memory

Alpha Ca(2+)/calmodulin-dependent kinase II (alphaCaMKII), the major synaptic protein in the forebrain, can switch into a state of autonomous activity upon autophosphorylation. It has been proposed that alphaCaMKII autophosphorylation mediates long-term memory (LTM) storage. However, recent evidence...

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Bibliographic Details
Published in:Trends in neurosciences (Regular ed.) 2006-08, Vol.29 (8), p.459-465
Main Authors: Irvine, Elaine E, von Hertzen, Laura S J, Plattner, Florian, Giese, Karl Peter
Format: Article
Language:English
Subjects:
Animals
Calcium-Calmodulin-Dependent Protein Kinase Kinase
Humans
Memory - physiology
Models, Biological
Phosphorylation
Protein Serine-Threonine Kinases - genetics
Protein Serine-Threonine Kinases - metabolism
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Summary:Alpha Ca(2+)/calmodulin-dependent kinase II (alphaCaMKII), the major synaptic protein in the forebrain, can switch into a state of autonomous activity upon autophosphorylation. It has been proposed that alphaCaMKII autophosphorylation mediates long-term memory (LTM) storage. However, recent evidence shows that synaptic stimulation and behavioural training only transiently increase the autonomous alphaCaMKII activity, implicating alphaCaMKII autophosphorylation in LTM formation rather than storage. Consistent with this, mutant mice deficient in alphaCaMKII autophosphorylation can store LTM after a massed training protocol, but cannot form LTM after a single trial. Here, we review evidence that the role of alphaCaMKII autophosphorylation is in fact to enable LTM formation after a single training trial, possibly by regulating LTM consolidation-specific transcription.
ISSN:0166-2236