The actin cytoskeleton differentially regulates NG115-401L cell ryanodine receptor and inositol 1,4,5-trisphosphate receptor induced calcium signaling pathways

Regulation of bi-directional communication between intracellular Ca2+ pools and surface Ca2+ channels remains incompletely characterized. We report Ca2+ release mediated by inositol 1,4,5-trisphosphate receptor (IP3R) and ryanodine receptor (RyR) pathways is diminished under actin cytoskeleton disru...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2009-02, Vol.379 (2), p.594-599
Main Authors: Bose, Diptiman D., Thomas, David W.
Format: Article
Language:English
Subjects:
Actin
Actins - metabolism
Animals
Ca2
Ca2+ influx
Ca2+ release
Calcium Signaling
Cell Line, Tumor
Cerebral Cortex - metabolism
Cytochalasin D - pharmacology
Cytoskeleton
Cytoskeleton - metabolism
Inositol 1,4,5-trisphosphate receptor
Inositol 1,4,5-Trisphosphate Receptors - metabolism
Oxazoles - pharmacology
Ryanodine receptor
Ryanodine Receptor Calcium Release Channel - metabolism
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Summary:Regulation of bi-directional communication between intracellular Ca2+ pools and surface Ca2+ channels remains incompletely characterized. We report Ca2+ release mediated by inositol 1,4,5-trisphosphate receptor (IP3R) and ryanodine receptor (RyR) pathways is diminished under actin cytoskeleton disruption in NG115-401L (401L) neuronal cells, yet despite truncated Ca2+ release, Ca2+ influx was not significantly altered in these experiments. However, disruption of cortical actin networks completely abolished IP3R induced Ca2+ release, whereas RyR-mediated Ca2+ release was preserved, albeit attenuated. Moreover, cortical actin disruption completely abolished IP3R and RyR linked Ca2+ influx even though Ca2+ pool sensitivities were different. These findings suggest discrete Ca2+ store/Ca2+ channel coupling mechanisms in the IP3R and RyR pathways as revealed by the differential sensitivity to actin perturbation.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2008.12.138