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

2009; Nature Portfolio; Volume: 458; Issue: 7236 Linguagem: Inglês

10.1038/nature07842

1476-4687

Seok-Jin R. Lee, Yasmin Escobedo-Lozoya, Erzsebet M. Szatmari, Ryohei Yasuda,

Retinal Development and Disorders

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. CaMKII, or Ca2+/calmodulin-dependent kinase II, is a signalling molecule that is critical for the induction of long-term potentiation (LTP), the enhanced communication between pairs of neurons thought to underlie some forms of learning and memory. Ryohei Yasuda's group at Duke University has developed a new imaging technology capable of tracking the activation of CaMKII within single synapses during LTP. The images show transient, channel-specific and compartmentalized activation of CaMKII in the synapses undergoing synaptic plasticity. This study has developed a new imaging technology to track the activation of CaMKII locally within an individual dendritic spine. CaMKII is transiently activated during synaptic potentiation and does not spread to neighbouring dendritic domains, thus ensuring that synaptic changes remain localized.