Protein kinase C mediated regulation of calcium channels in PC-12 pheochromocytoma cells

Katherine M. Harris; Sathapana Kongsamut; Richard J. Miller

doi:10.1016/0006-291X(86)90391-8

Protein kinase C mediated regulation of calcium channels in PC-12 pheochromocytoma cells

Katherine M. Harris^*, Sathapana Kongsamut, Richard J. Miller

^*Corresponding author for this work

Pharmacology

Research output: Contribution to journal › Article › peer-review

68 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	1298-1305
Number of pages	8
Journal	Biochemical and Biophysical Research Communications
Volume	134
Issue number	3
DOIs	https://doi.org/10.1016/0006-291X(86)90391-8
State	Published - Feb 13 1986

Funding

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.

ASJC Scopus subject areas

Molecular Biology
Biophysics
Biochemistry
Cell Biology

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title = "Protein kinase C mediated regulation of calcium channels in PC-12 pheochromocytoma cells",

abstract = "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.",

author = "Harris, \{Katherine M.\} and Sathapana Kongsamut and Miller, \{Richard J.\}",

note = "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.",

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AU - Miller, Richard J.

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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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Protein kinase C mediated regulation of calcium channels in PC-12 pheochromocytoma cells

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