title: alphaCaMKII autophosphorylation: a fast track to memory.
abstract: 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.
authors.affiliation: Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.
authors.forename: Elaine E
authors.initials: EE
authors.lastname: Irvine
authors.forename: Laura S J
authors.initials: LS
authors.lastname: von Hertzen
authors.forename: Florian
authors.initials: F
authors.lastname: Plattner
authors.forename: Karl Peter
authors.initials: KP
authors.lastname: Giese
mesh_terms: D000818:Animals; D054737:Calcium-Calmodulin-Dependent Protein Kinase Kinase; D006801:Humans; D008568:Memory / Q000502:physiology*; D008954:Models, Biological; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*
chemical_list: D017346:Protein Serine-Threonine Kinases; D054737:Calcium-Calmodulin-Dependent Protein Kinase Kinase