| First Author | Chang JY | Year | 2019 |
| Journal | Nat Commun | Volume | 10 |
| Issue | 1 | Pages | 2784 |
| PubMed ID | 31239443 | Mgi Jnum | J:280827 |
| Mgi Id | MGI:6323831 | Doi | 10.1038/s41467-019-10694-z |
| Citation | Chang JY, et al. (2019) Mechanisms of Ca(2+)/calmodulin-dependent kinase II activation in single dendritic spines. Nat Commun 10(1):2784 |
| abstractText | CaMKIIalpha plays an essential role in decoding Ca(2+) signaling in spines by acting as a leaky Ca(2+) integrator with the time constant of several seconds. However, the mechanism by which CaMKIIalpha integrates Ca(2+) signals remains elusive. Here, we imaged CaMKIIalpha-CaM association in single dendritic spines using a new FRET sensor and two-photon fluorescence lifetime imaging. In response to a glutamate uncaging pulse, CaMKIIalpha-CaM association increases in ~0.1 s and decays over ~3 s. During repetitive glutamate uncaging, which induces spine structural plasticity, CaMKIIalpha-CaM association did not show further increase but sustained at a constant level. Since CaMKIIalpha activity integrates Ca(2+) signals over ~10 s under this condition, the integration of Ca(2+) signal by CaMKIIalpha during spine structural plasticity is largely due to Ca(2+)/CaM-independent, autonomous activity. Based on these results, we propose a simple kinetic model of CaMKIIalpha activation in dendritic spines. |
