1. Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA

Correspondence to: Ryohei Yasuda¹ Correspondence and requests for materials should be addressed to R.Y. (Email: yasuda@neuro.duke.edu).

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.

1. Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA

Correspondence to: Ryohei Yasuda¹ Correspondence and requests for materials should be addressed to R.Y. (Email: yasuda@neuro.duke.edu).

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