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

Author

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  • Jui-Yun Chang

    (Duke University
    Max Planck Florida Institute for Neuroscience)

  • Yoshihisa Nakahata

    (Max Planck Florida Institute for Neuroscience)

  • Yuki Hayano

    (Max Planck Florida Institute for Neuroscience)

  • Ryohei Yasuda

    (Max Planck Florida Institute for Neuroscience)

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.

Suggested Citation

  • Jui-Yun Chang & Yoshihisa Nakahata & Yuki Hayano & Ryohei Yasuda, 2019. "Mechanisms of Ca2+/calmodulin-dependent kinase II activation in single dendritic spines," Nature Communications, Nature, vol. 10(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-10694-z
    DOI: 10.1038/s41467-019-10694-z
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