Involvement of calciseptine-sensitive calcium channels in the evoked acetylcholine release from electric organ synaptosomes

Biol Pharm Bull. 1997 Jun;20(6):641-5. doi: 10.1248/bpb.20.641.

Abstract

The high K(+)-evoked release of acetylcholine (ACh) from electric organ synaptosomes isolated from the Japanese marine ray, Narke japonica, was strongly inhibited by dihydropyridines at micromolar concentrations. However, this inhibition seems to be a non-specific effect since the agonist (-)-Bay K 8644 also had inhibitory effects. Calciseptine, a peptide toxin specific for L-type Ca channels, inhibited to a lesser extent the evoked acetylcholine release: the maximum inhibition was about 20%. This finding is in accord with our data (Tokumaru et al., J. Neurochem., 65, 831(1995)) regarding inhibition by a monoclonal antibody against the alpha 2 delta-subunit of the L-type Ca channel and provides evidence for the involvement of an L-type-like Ca channel in ACh release in addition to omega-conotoxin GVIA-sensitive N-type and omega-agatoxin IVA-sensitive P-type Ca channels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / antagonists & inhibitors*
  • Animals
  • Calcium Channels / drug effects
  • Calcium Channels / metabolism*
  • Dihydropyridines / pharmacology
  • Elapid Venoms / pharmacology*
  • Electric Organ / metabolism*
  • Potassium Chloride / pharmacology
  • Skates, Fish
  • Synaptosomes / metabolism*

Substances

  • Calcium Channels
  • Dihydropyridines
  • Elapid Venoms
  • calciseptine
  • Potassium Chloride
  • Acetylcholine