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Neuropharmacology. 1994 Feb;33(2):251-4.

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

Author information

1
Department of Neuropsychopharmacology, Nagoya University School of Medicine, Japan.

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.

PMID:
8035911
DOI:
10.1016/0028-3908(94)90016-7
[Indexed for MEDLINE]

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