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 | |
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