Inhibition of endogenous glutamate release from hippocampal tissue by Ca2+ channel toxins

Eur J Pharmacol. 1993 Jul 20;238(2-3):383-6. doi: 10.1016/0014-2999(93)90870-n.


The pharmacology of voltage-dependent Ca2+ channels involved in the release of endogenous neurotransmitter amino acids was measured from small tissue slices of rat hippocampal CA1 region. Application of 50 mM KCl induced large increases in Ca(2+)-dependent overflow of endogenous glutamate, aspartate and gamma-aminobutyric acid (GABA). Pretreatment of tissues with the funnel-web spider toxin omega-Aga-IVA (200 nM) reduced KCl-induced overflow of all three amino acids. Pretreatment with the cone snail toxin omega-CgTx-GVIA (2 microM) caused similar but smaller reductions in amino acid overflow (aspartate overflow was not reduced significantly). These results indicate that P-type Ca2+ channels, and to a lesser extent, N-type Ca2+ channels, are involved in the release of transmitter amino acids under these conditions.

MeSH terms

  • Animals
  • Aspartic Acid / metabolism
  • Calcium Channel Blockers / pharmacology*
  • Calcium Channels / drug effects
  • Chromatography, High Pressure Liquid
  • Glutamates / metabolism*
  • Glutamic Acid
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Neurotransmitter Agents / metabolism*
  • Peptides / pharmacology
  • Potassium Chloride / pharmacology*
  • Rats
  • Spider Venoms / pharmacology
  • gamma-Aminobutyric Acid / metabolism
  • omega-Agatoxin IVA
  • omega-Conotoxin GVIA


  • Calcium Channel Blockers
  • Calcium Channels
  • Glutamates
  • Neurotransmitter Agents
  • Peptides
  • Spider Venoms
  • omega-Agatoxin IVA
  • Aspartic Acid
  • Glutamic Acid
  • gamma-Aminobutyric Acid
  • Potassium Chloride
  • omega-Conotoxin GVIA