Mechanisms of Ca2+/calmodulin-dependent kinase II activation in single dendritic spines

Jui-Yun Chang, Yoshihisa Nakahata, Yuki Hayano and Ryohei Yasuda ()
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Jui-Yun Chang: Duke University
Yoshihisa Nakahata: Max Planck Florida Institute for Neuroscience
Yuki Hayano: Max Planck Florida Institute for Neuroscience
Ryohei Yasuda: Max Planck Florida Institute for Neuroscience

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: Abstract CaMKIIα plays an essential role in decoding Ca2+ signaling in spines by acting as a leaky Ca2+ integrator with the time constant of several seconds. However, the mechanism by which CaMKIIα integrates Ca2+ signals remains elusive. Here, we imaged CaMKIIα-CaM association in single dendritic spines using a new FRET sensor and two-photon fluorescence lifetime imaging. In response to a glutamate uncaging pulse, CaMKIIα-CaM association increases in ~0.1 s and decays over ~3 s. During repetitive glutamate uncaging, which induces spine structural plasticity, CaMKIIα-CaM association did not show further increase but sustained at a constant level. Since CaMKIIα activity integrates Ca2+ signals over ~10 s under this condition, the integration of Ca2+ signal by CaMKIIα during spine structural plasticity is largely due to Ca2+/CaM-independent, autonomous activity. Based on these results, we propose a simple kinetic model of CaMKIIα activation in dendritic spines.

Date: 2019
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DOI: 10.1038/s41467-019-10694-z

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