Journal
NATURE
Volume 458, Issue 7236, Pages 299-U58Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature07842
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Funding
- Burroughs Wellcome Fund
- Dana Foundation
- Alfred P. Sloan Foundation
- Autism Speaks
- National Alliance of Autism Research
- Whitehall Foundation
- Alzheimer's Association
- National Institute of Mental Health [R01MH08004]
- National Science Foundation [0642000]
- Duke University Undergraduate Research Support Grants
- Howard Hughes Neuroscience Forum Fellowship
- Ruth K. Broad Biomedical Research Foundation
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [0642000] Funding Source: National Science Foundation
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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 (similar to 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.
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