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

Abstract

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.

• Authors: K Yamada, T Teraoka, S Morita, T Hasegawa, T Nabeshima
• Journal: Neuropharmacology (Neuropharmacology) Vol. 33 Issue 2 Pg. 251-4 (Feb 1994) ISSN: 0028-3908 [Print] England
• PMID: 8035911 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

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

Topics

• Animals
• Body Temperature (drug effects)
• Brain (cytology, 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, toxicity)
• Rats
• Rats, Wistar
• omega-Conotoxin GVIA