Omega-conotoxin GVIA protects against ischemia-induced neuronal death in the Mongolian gerbil but not against quinolinic acid-induced neurotoxicity in the rat

Neuropharmacology. 1994 Feb;33(2):251-4. doi: 10.1016/0028-3908(94)90016-7.


Excessive release of neurotransmitters is reported to contribute to the delayed neuronal death in animal models of cerebral ischemia. Since evidence is accumulating that N-type voltage-sensitive calcium channels (N-channels) regulate the release of neurotransmitters, we investigated the effects of omega-conotoxin GVIA (omega-CTX), an antagonist of N-channels, on delayed neuronal death following transient ischemia in gerbils. Delayed neuronal death in the CA1 subfield of the hippocampus following 5-min ischemia was attenuated by omega-CTX in a dose-dependent manner when the agent was injected intracisternally 1 hr before ischemia was produced. However, omega-CTX failed to prevent neurotoxicity produced by a direct injection of quinolinic acid into the hippocampus in rats. These results suggest that omega-CTX has a neuroprotective effect against ischemic brain injury, which effect probably results from its inhibition of the excessive release of neurotransmitters, including excitatory amino acids, during ischemia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Body Temperature / drug effects
  • Brain / cytology
  • Brain / drug effects*
  • Calcium Channel Blockers / pharmacology*
  • Cell Death / drug effects
  • Gerbillinae
  • Hippocampus / drug effects
  • Ischemic Attack, Transient / pathology*
  • Male
  • Neurons / drug effects
  • Peptides / pharmacology*
  • Quinolinic Acid / antagonists & inhibitors*
  • Quinolinic Acid / toxicity
  • Rats
  • Rats, Wistar
  • omega-Conotoxin GVIA


  • Calcium Channel Blockers
  • Peptides
  • omega-Conotoxin GVIA
  • Quinolinic Acid