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.
You may also like
Modeling the turtle brain provides insights: Routing...
February 15, 2023Max Planck Institute for Brain Research
Amygdala Intercalated Cells: Gatekeepers and Conveyors...
January 19, 2023Max Planck Florida Institute for Neuroscience
Aversive bimodal associations differently impact...
January 19, 2023Max Planck Institute for Chemical Ecology
In the zone for memories
January 10, 2023Max Planck Institute for Brain Research
Commonalities and Asymmetries in the Neurobiological...
January 5, 2023Max Planck Institute for Psycholinguistics
A hierarchy of linguistic predictions during natural...
January 5, 2023Max Planck Institute for Psycholinguistics