Protective Effect of Zinc Against Ischemic Neuronal Injury in a Middle Cerebral Artery Occlusion Model
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- Kitamura Youji
- Graduate School of Medicine and Dentistry and Pharmaceutical Sciences, Okayama University, Japan
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- Iida Yasuhiko
- Department of Bioimaging, Medical Sciences, Gunma University, Japan
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- Abe Jun
- Department of Patho-functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan
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- Ueda Masashi
- Department of Patho-functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan
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- Mifune Masaki
- Graduate School of Medicine and Dentistry and Pharmaceutical Sciences, Okayama University, Japan
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- Kasuya Fumiyo
- Department of Toxicology, Pharmaceutical Sciences, Kobegakuin University, Japan
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- Ohta Masayuki
- Department of Toxicology, Pharmaceutical Sciences, Kobegakuin University, Japan
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- Igarashi Kazuo
- Department of Chemistry, Virginia Polytechnic Institute and State University, USA
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- Saito Yutaka
- Graduate School of Medicine and Dentistry and Pharmaceutical Sciences, Okayama University, Japan
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- Saji Hideo
- Department of Patho-functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan
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In this study, we investigated the effect of vesicular zinc on ischemic neuronal injury. In cultured neurons, addition of a low concentration (under 100 μM) of zinc inhibited both glutamate-induced calcium influx and neuronal death. In contrast, a higher concentration (over 150 μM) of zinc decreased neuronal viability, although calcium influx was inhibited. These results indicate that zinc exhibits biphasic effects depending on its concentration. Furthermore, in cultured neurons, co-addition of glutamate and CaEDTA, which binds extra-cellular zinc, increased glutamate-induced calcium influx and aggravated the neurotoxicity of glutamate. In a rat transient middle cerebral artery occlusion (MCAO) model, the infarction volume, which is related to the neurotoxicity of glutamate, increased rapidly on the intracerebral ventricular injection of CaEDTA 30 min prior to occlusion. These results suggest that zinc released from synaptic vesicles may provide a protective effect against ischemic neuronal injury.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 100 (2), 142-148, 2006
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680154284544
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- NII論文ID
- 10018240763
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 7821858
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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