Protein kinase C modulates the release of [3H]5-hydroxytryptamine in the spinal cord of the rat: The role of L-type voltage-dependent calcium channels

Vijayalakshmi C. Gandhi, D. J. Jones

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

The present studies examined the relationship between protein kinase C (PKC) and L-type voltage-dependent calcium channels in modulating the release of neurotransmitter from K+-depolarized rat spinal cord synaptosomes. Activators of PKC, such as phorbol 12-myristate 13-acetate (PMA), mezerein and oleoyl acetylglycerol produced a concentration-dependent potentiation of K+-induced release of [3H]5-hydroxytryptamine ([3H]5-HT). Enhanced release was dependent on the concentration of both Ca2+ and K+ in the superfusion medium. Calcium-independent release of [3H]5-HT or release induced by the Ca2+ ionophore were unaffected by PKC activators. Calcium-dependent release of [3H]5-HT, evoked by K+, was enhanced under similar conditions by the L-type Ca2+ channel agonists Bay K 8644 and (+)-SDZ 202-791. Nimodipine, an L-type Ca2+ channel antagonist, while having no independent effect on K+-induced release of [3H]5-HT, abolished the potentiative effects of Bay K 8644 and PMA. Similarly, the PKC inhibitors, polymyxin B and staurosporine, blocked effects of both PMA and Bay K 8644 on K+-stimulated release of [3H]5-HT. Neither PMA nor Bay K 8644 altered the uptake of [3H]5-HT. These results suggest that PKC-dependent mechanisms utilize calcium influx, via the L-type calcium channel, to modulate release of neurotransmitter and indicate a possible functional link between PKC and L-type voltage-dependent calcium channels in the spinal cord.

Original languageEnglish (US)
Pages (from-to)1101-1109
Number of pages9
JournalNeuropharmacology
Volume31
Issue number11
DOIs
StatePublished - Nov 1992

Keywords

  • L-type calcium channels
  • autoreceptors
  • phorbol esters
  • protein kinase C
  • rat spinal cord
  • serotonin release
  • synaptosomes

ASJC Scopus subject areas

  • Pharmacology
  • Cellular and Molecular Neuroscience

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