αCaMKII autophosphorylation: a fast track to memory

Elaine E. Irvine, Laura S J von Hertzen, Florian Plattner, Karl Peter Giese

Research output: Contribution to journalReview article

75 Scopus citations

Abstract

Alpha Ca2+/calmodulin-dependent kinase II (αCaMKII), the major synaptic protein in the forebrain, can switch into a state of autonomous activity upon autophosphorylation. It has been proposed that αCaMKII autophosphorylation mediates long-term memory (LTM) storage. However, recent evidence shows that synaptic stimulation and behavioural training only transiently increase the autonomous αCaMKII activity, implicating αCaMKII autophosphorylation in LTM formation rather than storage. Consistent with this, mutant mice deficient in αCaMKII 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 αCaMKII autophosphorylation is in fact to enable LTM formation after a single training trial, possibly by regulating LTM consolidation-specific transcription.

Original languageEnglish (US)
Pages (from-to)459-465
Number of pages7
JournalTrends in Neurosciences
Volume29
Issue number8
DOIs
StatePublished - Aug 1 2006

ASJC Scopus subject areas

  • Neuroscience(all)

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    Irvine, E. E., von Hertzen, L. S. J., Plattner, F., & Giese, K. P. (2006). αCaMKII autophosphorylation: a fast track to memory. Trends in Neurosciences, 29(8), 459-465. https://doi.org/10.1016/j.tins.2006.06.009