αCaMKII autophosphorylation: a fast track to memory

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

Research output: Contribution to journalArticle

70 Citations (Scopus)

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 2006

Fingerprint

Calcium-Calmodulin-Dependent Protein Kinases
Long-Term Memory
Prosencephalon
Proteins

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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

αCaMKII autophosphorylation : a fast track to memory. / Irvine, Elaine E.; von Hertzen, Laura S J; Plattner, Florian; Giese, Karl Peter.

In: Trends in Neurosciences, Vol. 29, No. 8, 08.2006, p. 459-465.

Research output: Contribution to journalArticle

Irvine, EE, von Hertzen, LSJ, Plattner, F & Giese, KP 2006, 'αCaMKII autophosphorylation: a fast track to memory', Trends in Neurosciences, vol. 29, no. 8, pp. 459-465. https://doi.org/10.1016/j.tins.2006.06.009
Irvine EE, von Hertzen LSJ, Plattner F, Giese KP. αCaMKII autophosphorylation: a fast track to memory. Trends in Neurosciences. 2006 Aug;29(8):459-465. https://doi.org/10.1016/j.tins.2006.06.009
Irvine, Elaine E. ; von Hertzen, Laura S J ; Plattner, Florian ; Giese, Karl Peter. / αCaMKII autophosphorylation : a fast track to memory. In: Trends in Neurosciences. 2006 ; Vol. 29, No. 8. pp. 459-465.
@article{cf281ab84d48446796814cf73d1c4b46,
title = "αCaMKII autophosphorylation: a fast track to memory",
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.",
author = "Irvine, {Elaine E.} and {von Hertzen}, {Laura S J} and Florian Plattner and Giese, {Karl Peter}",
year = "2006",
month = "8",
doi = "10.1016/j.tins.2006.06.009",
language = "English (US)",
volume = "29",
pages = "459--465",
journal = "Trends in Neurosciences",
issn = "0378-5912",
publisher = "Elsevier Limited",
number = "8",

}

TY - JOUR

T1 - αCaMKII autophosphorylation

T2 - a fast track to memory

AU - Irvine, Elaine E.

AU - von Hertzen, Laura S J

AU - Plattner, Florian

AU - Giese, Karl Peter

PY - 2006/8

Y1 - 2006/8

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=33746373482&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33746373482&partnerID=8YFLogxK

U2 - 10.1016/j.tins.2006.06.009

DO - 10.1016/j.tins.2006.06.009

M3 - Article

C2 - 16806507

AN - SCOPUS:33746373482

VL - 29

SP - 459

EP - 465

JO - Trends in Neurosciences

JF - Trends in Neurosciences

SN - 0378-5912

IS - 8

ER -