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

K. Yamada, T. Teraoka, S. Morita, T. Hasegawa, Toshitaka Nabeshima

Research output: Contribution to journalArticle

34 Citations (Scopus)

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 ω-conotoxin GVIA (ω-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 ω-CTX in a dose-dependent manner when the agent was injected intracisternally 1 hr before ischemia was produced. However, ω-CTX failed to prevent neurotoxicity produced by a direct injection of quinolinic acid into the hippocampus in rats. These results suggest that ω-CTX has a neuroprotective effect against ischemie brain injury, which effect probably results from its inhibition of the excessive release of neurotransmitters, including excitatory amino acids, during ischemia.

Original languageEnglish
Pages (from-to)251-254
Number of pages4
JournalNeuropharmacology
Volume33
Issue number2
DOIs
Publication statusPublished - 01-01-1994
Externally publishedYes

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Conotoxins
Quinolinic Acid
Gerbillinae
Ischemia
Neurotransmitter Agents
Calcium Channels
Hippocampus
Excitatory Amino Acids
Neuroprotective Agents
Brain Ischemia
Brain Injuries
Animal Models
Injections

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Cellular and Molecular Neuroscience

Cite this

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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 ω-conotoxin GVIA (ω-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 ω-CTX in a dose-dependent manner when the agent was injected intracisternally 1 hr before ischemia was produced. However, ω-CTX failed to prevent neurotoxicity produced by a direct injection of quinolinic acid into the hippocampus in rats. These results suggest that ω-CTX has a neuroprotective effect against ischemie brain injury, which effect probably results from its inhibition of the excessive release of neurotransmitters, including excitatory amino acids, during ischemia.",
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ω-conotoxin GVIA protects against ischemia-induced neuronal death in the Mongolian gerbil but not against quinolinic acid-induced neurotoxicity in the rat. / Yamada, K.; Teraoka, T.; Morita, S.; Hasegawa, T.; Nabeshima, Toshitaka.

In: Neuropharmacology, Vol. 33, No. 2, 01.01.1994, p. 251-254.

Research output: Contribution to journalArticle

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