TY - JOUR
T1 - ω-conotoxin GVIA protects against ischemia-induced neuronal death in the Mongolian gerbil but not against quinolinic acid-induced neurotoxicity in the rat
AU - Yamada, K.
AU - Teraoka, T.
AU - Morita, S.
AU - Hasegawa, T.
AU - Nabeshima, Toshitaka
N1 - Funding Information:
Acknowledgements-This study was supportedb y a Grant-in-Aid for Science Research( Nos 00092093, 033040a3n6d 05454148)f rom the Ministry of Education, Science and Culture, Japan.
PY - 1994/2
Y1 - 1994/2
N2 - 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.
AB - 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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U2 - 10.1016/0028-3908(94)90016-7
DO - 10.1016/0028-3908(94)90016-7
M3 - Article
C2 - 8035911
AN - SCOPUS:0028174640
SN - 0028-3908
VL - 33
SP - 251
EP - 254
JO - Neuropharmacology
JF - Neuropharmacology
IS - 2
ER -