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
N1 - Funding Information:
We thank T.V.P. Bliss, P.W. Frankland, J.E. Lisman, N. Otmakhov, J. Vernon and members of our laboratory for critical reading of the manuscript. This work was supported by the Biotechnology and Biological Sciences Research Council, the Medical Research Council and the Wellcome Trust.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
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.
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U2 - 10.1016/j.tins.2006.06.009
DO - 10.1016/j.tins.2006.06.009
M3 - Review article
C2 - 16806507
AN - SCOPUS:33746373482
SN - 0166-2236
VL - 29
SP - 459
EP - 465
JO - Trends in Neurosciences
JF - Trends in Neurosciences
IS - 8
ER -