Activation of CaMKII in single dendritic spines during long-term potentiation

Seok-Jin R. Lee, Yasmin Escobedo-Lozoya, Erzsebet M. Szatmari and Ryohei Yasuda ()
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Seok-Jin R. Lee: Duke University Medical Center, Durham, North Carolina 27710, USA
Yasmin Escobedo-Lozoya: Duke University Medical Center, Durham, North Carolina 27710, USA
Erzsebet M. Szatmari: Duke University Medical Center, Durham, North Carolina 27710, USA
Ryohei Yasuda: Duke University Medical Center, Durham, North Carolina 27710, USA

Nature, 2009, vol. 458, issue 7236, 299-304

Abstract: Abstract Calcium/calmodulin-dependent kinase II (CaMKII) plays a central part in long-term potentiation (LTP), which underlies some forms of learning and memory. Here we monitored the spatiotemporal dynamics of CaMKII activation in individual dendritic spines during LTP using two-photon fluorescence lifetime imaging microscopy, in combination with two-photon glutamate uncaging. Induction of LTP and associated spine enlargement in single spines triggered transient (∼1 min) CaMKII activation restricted to the stimulated spines. CaMKII in spines was specifically activated by NMDA receptors and L-type voltage-sensitive calcium channels, presumably by nanodomain Ca2+ near the channels, in response to glutamate uncaging and depolarization, respectively. The high degree of compartmentalization and channel specificity of CaMKII signalling allow stimuli-specific spatiotemporal patterns of CaMKII signalling and may be important for synapse-specificity of synaptic plasticity.

Date: 2009
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DOI: 10.1038/nature07842

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