TY - JOUR
T1 - Protein kinase C mediated regulation of calcium channels in PC-12 pheochromocytoma cells
AU - Harris, Katherine M.
AU - Kongsamut, Sathapana
AU - Miller, Richard J.
N1 - Funding Information:
This work was supported by NIH grants MH 40165-OlAl to R.J.M. and grants from and the Brain Research Institute of the S.K. was supported by a grant from the The authors would like to thank Dr. generously supplying BAY K8644 and Della the manuscript.
PY - 1986/2/13
Y1 - 1986/2/13
N2 - Depolarization of PC-12 pheochromocytoma cells with K+ produces an immediate increase in catecholamine release. The stimulation of release is blocked by Co2+, removal of extracellular Ca2+ or by dihydropyridine drugs such as nitrendipine. Release is enhanced by other dihydropyridines such as BAY K8644. Release is accompanied by a voltage dependent uptake of 45Ca2+ which is also blocked by Co2+ or nitrendipine and enhanced by BAY K8644. The phorbol ester phorbol 12-myristate-13-acetate (TPA) in the range 10-9 - 10-6 M produced little effect by itself but augmented the K+ evoked release of catecholamine. An analog of TPA which does not activate protein kinase C was ineffective. In contrast, TPA in the same concentration range blocked influx of 45Ca2+ induced by 70 mM K+ or 70 mM K+/ BAY K8644. 45Ca2+ influx produced by A23187 was not blocked by TPA. The results suggest a system by which protein kinase C may regulate the output of transmitters from secretory cells.
AB - Depolarization of PC-12 pheochromocytoma cells with K+ produces an immediate increase in catecholamine release. The stimulation of release is blocked by Co2+, removal of extracellular Ca2+ or by dihydropyridine drugs such as nitrendipine. Release is enhanced by other dihydropyridines such as BAY K8644. Release is accompanied by a voltage dependent uptake of 45Ca2+ which is also blocked by Co2+ or nitrendipine and enhanced by BAY K8644. The phorbol ester phorbol 12-myristate-13-acetate (TPA) in the range 10-9 - 10-6 M produced little effect by itself but augmented the K+ evoked release of catecholamine. An analog of TPA which does not activate protein kinase C was ineffective. In contrast, TPA in the same concentration range blocked influx of 45Ca2+ induced by 70 mM K+ or 70 mM K+/ BAY K8644. 45Ca2+ influx produced by A23187 was not blocked by TPA. The results suggest a system by which protein kinase C may regulate the output of transmitters from secretory cells.
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U2 - 10.1016/0006-291X(86)90391-8
DO - 10.1016/0006-291X(86)90391-8
M3 - Article
C2 - 2418837
AN - SCOPUS:0022575988
SN - 0006-291X
VL - 134
SP - 1298
EP - 1305
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -