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Chronic activation of protein kinase C by phorbol ester reduces calcium channel expression in chick sympathetic neurons.

Authors
  • Przywara, D A
  • Zhong, H
  • Kulkarni, J S
  • Anderson, G F
  • Wakade, A R
Type
Published Article
Journal
Neuroscience Letters
Publisher
Elsevier
Publication Date
Jun 27, 1997
Volume
229
Issue
2
Pages
138–140
Identifiers
PMID: 9223610
Source
Medline
License
Unknown

Abstract

Chronic activation of protein kinase C (PKC) has been implicated in regulation of Ca2+ entry responsible for normal development of transmitter properties in cultured sympathetic neurons. The idea that PKC alters the expression of Ca2+ channels was tested using phorbol 12,13-dibutyrate (PDB) which activates PKC and also supports survival of chick sympathetic neurons in the absence of nerve growth factor (NGF). Whole cell voltage-clamp showed that neurons supported by PDB for 2 days had significantly lower Ca2+ current density (0.243 +/- 0.025 pA/microm2) than those supported by NGF (0.356 +/- 0.033 pA/microm2). [125I]omega-Conotoxin GVIA binding showed that PDB-supported neurons had significantly lower maximum binding (617 +/- 223 fmol/mg protein) compared with those supported by NGF (1099 +/- 192 fmol/mg protein). These results support the conclusion that chronic activation of PKC limits the expression of N-type Ca2+ channels. A reduction in Ca2+ channel number is consistent with, and could account for the mature type Ca2+ handling and transmitter release properties seen in sympathetic neuro-effector preparations, sympathetic neurons co-cultured with their targets, and neurons supported by PDB.

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