Brain voltage-sensitive calcium channel subtypes differentiated by ω-conotoxin fraction GVIA Academic Article Article uri icon


MeSH Major

  • Calcitonin Gene-Related Peptide
  • Immunity, Innate
  • Neurons
  • Signal Transduction
  • Skin


  • We have studied the voltage-activated influx of Ca2+ into synaptosomes. Rapid 45Ca2+ influx into synaptosomes, measured at 1 sec, was blocked by predepolarization and by low concentrations of cadmium (IC50, 1 microM), as anticipated for voltage-sensitive calcium channels (VSCCs). However, fluxes were insensitive to dihydropyridine drugs that block or activate VSCCs, including nitrendipine, Bay K 8644, and (+)- and (-)-PN202-791. Phenylalkylamine calcium antagonists, including verapamil and desmethoxyverapamil, blocked 45Ca2+ uptake in a nonspecific fashion. The peptide omega-conotoxin fraction GVIA (omega-CgTx GVIA) blocked 45Ca2+ uptake in a biphasic fashion, with a 30% reduction at 50 pM toxin and a further decrease at concentrations greater than 5 nM. The toxin inhibited neurotransmitter release from synaptosomes in nanomolar concentrations, corresponding to its low-affinity effects on 45Ca2+ influx. omega-CgTx GVIA also inhibited depolarization-induced increases in intracellular Ca2+ concentration in single hippocampal and striatal neurons. These findings indicate that omega-CgTx GVIA blocks VSCCs in both cell bodies and nerve terminals and that the predominant form of VSCC in nerve terminals is the dihydropyridine-insensitive N type.

publication date

  • December 1986



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1073/pnas.83.22.8804

PubMed ID

  • 2430302

Additional Document Info

start page

  • 8804

end page

  • 7


  • 83


  • 22