The actin cytoskeleton differentially regulates NG115-401L cell ryanodine receptor and inositol 1,4,5-trisphosphate receptor induced calcium signaling pathways |
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| Authors: | Diptiman D. Bose |
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| Affiliation: | a Department of Molecular Biosciences School of Veterinary Medicine, University of California, Davis, CA 95616, United States
b Department of Physiology and Pharmacology, Thomas J. Long School of Pharmacy and Health Sciences, University of the Pacific, Stockton, CA 95211, United States |
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| Abstract: | 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. |
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| Keywords: | Ca2+ Actin Cytoskeleton Inositol 1,4,5-trisphosphate receptor Ryanodine receptor Ca2+ release Ca2+ influx |
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