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 Ca(2+) pools and surface Ca(2+) channels remains incompletely characterized. We report Ca(2+) release mediated by inositol 1,4,5-trisphosphate receptor (IP(3)R) and ryanodine receptor (RyR) pathways is diminished under actin cytoskeleton disruption in NG115-401L (401L) neuronal cells, yet despite truncated Ca(2+) release, Ca(2+) influx was not significantly altered in these experiments. However, disruption of cortical actin networks completely abolished IP(3)R induced Ca(2+) release, whereas RyR-mediated Ca(2+) release was preserved, albeit attenuated. Moreover, cortical actin disruption completely abolished IP(3)R and RyR linked Ca(2+) influx even though Ca(2+) pool sensitivities were different. These findings suggest discrete Ca(2+) store/Ca(2+) channel coupling mechanisms in the IP(3)R and RyR pathways as revealed by the differential sensitivity to actin perturbation.
Bose
Diptiman D
DD
Department of Molecular Biosciences School of Veterinary Medicine, University of California, Davis, CA 95616, USA.
Thomas
David W
DW
D000199:Actins / Q000378:metabolism*; D000818:Animals; D020013:Calcium Signaling; D045744:Cell Line, Tumor; D002540:Cerebral Cortex / Q000378:metabolism; D015638:Cytochalasin D / Q000494:pharmacology; D003599:Cytoskeleton / Q000378:metabolism; D053496:Inositol 1,4,5-Trisphosphate Receptors / Q000378:metabolism*; D008387:Marine Toxins; D010080:Oxazoles / Q000494:pharmacology; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*
D000199:Actins; D053496:Inositol 1,4,5-Trisphosphate Receptors; D008387:Marine Toxins; D010080:Oxazoles; D019837:Ryanodine Receptor Calcium Release Channel; D015638:Cytochalasin D; C059041:calyculin A