*Present address: Department of Pharmacology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814–4799, USA.
Calcium-triggered exit of F-actin and IP3 3-kinase A from dendritic spines is rapid and reversible
Article first published online: 13 NOV 2006
European Journal of Neuroscience
Volume 24, Issue 9, pages 2491–2503, November 2006
How to Cite
Schell, M. J. and Irvine, R. F. (2006), Calcium-triggered exit of F-actin and IP3 3-kinase A from dendritic spines is rapid and reversible. European Journal of Neuroscience, 24: 2491–2503. doi: 10.1111/j.1460-9568.2006.05125.x
- Issue published online: 13 NOV 2006
- Article first published online: 13 NOV 2006
- Received 20 April 2006, revised 2 August 2006, accepted 19 August 2006
The structure of the actin cytoskeleton in dendritic spines is thought to underlie some forms of synaptic plasticity. We have used fixed and live-cell imaging in rat primary hippocampal cultures to characterize the synaptic dynamics of the F-actin binding protein inositol trisphosphate 3-kinase A (IP3K), which is localized in the spines of pyramidal neurons derived from the CA1 region. IP3K was intensely concentrated as puncta in spine heads when Ca2+ influx was low, but rapidly and reversibly redistributed to a striated morphology in the main dendrite when Ca2+ influx was high. Glutamate stimulated the exit of IP3K from spines within 10 s, and re-entry following blockage of Ca2+ influx commenced within a minute; IP3K appeared to remain associated with F-actin throughout this process. Ca2+-triggered F-actin relocalization occurred in about 90% of the cells expressing IP3K endogenously, and was modulated by the synaptic activity of the cultures, suggesting that it is a physiological process. F-actin relocalization was blocked by cytochalasins, jasplakinolide and by the over-expression of actin fused to green fluorescent protein. We also used deconvolution microscopy to visualize the relationship between F-actin and endoplasmic reticulum inside dendritic spines, revealing a delicate microorganization of IP3K near the Ca2+ stores. We conclude that Ca2+ influx into the spines of CA1 pyramidal neurons triggers the rapid and reversible retraction of F-actin from the dendritic spine head. This process contributes to changes in spine F-actin shape and content during synaptic activity, and might also regulate spine IP3 signals.