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

Abstract

Ca2+ / Calmodulin-dependent kinase II (CaMKII) plays a central role 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 2-photon fluorescence lifetime imaging microscopy in combination with 2-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 via 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.