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Complestatin antagonizee the AMPA/Kainate-induced neurotoxicity in cultured chick telencephalic neurons

Authors
 Ick Dong Yoo  ;  Bong Sik Yun  ;  In Ja Ryoo  ;  Soo Young Lee  ;  Myeong Heon Shin  ;  Seikwan Oh 
Citation
 NEUROCHEMICAL RESEARCH, Vol.27(4) : 337-343, 2002 
Journal Title
NEUROCHEMICAL RESEARCH
ISSN
 0364-3190 
Issue Date
2002
MeSH
Animals ; Cells,Cultured ; ChickEmbryo ; Chickens ; Chlorophenols/pharmacology* ; Excitatory Amino Acid Antagonists/pharmacology ; Kainic Acid/pharmacology ; Neurons/drug effects ; Neurons/physiology* ; Oligopeptides/pharmacology* ; Peptides, Cyclic* ; Phorbol 12,13-Dibutyrate/pharmacology ; Quinoxalines/pharmacology* ; Receptors,AMPA/antagonists & inhibitors* ; Receptors, Kainic Acid/antagonists & inhibitors* ; Staurosporine/pharmacology ; Telencephalon/physiology* ; Time Factors ; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology
Keywords
Complestatin ; AMPA/kainite ; chick neuron ; neurotoxicity
Abstract
Excitatory amino acids are known to induce considerable neurotoxicity in central nervous system. In the present study, the neurotoxicity was induced by application of kainate or AMPA in chick telencephalic neuron, and neuroprotective activity was tested with complestatin that was isolated from streptomyces species. In cultured telencephalic neurons exposed to 500 microM kainate for 2 days, the AMPA/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 5 microM) completely blocked kainate-induced neurotoxicity. Also, complestatin (0.5 microM) completely blocked kainate-induced neuronal injury at a concentration lower than that required for prototype AMPA/kainate receptor antagonist DNQX. In addition, complestatin blocked AMPA-induced neurotoxicity when the neurons were pretreated with cyclothiazide, a desensitization blocker of AMPA receptor. Surprisingly, when the onset of the treatment was delayed for 6 hours, complestatin led to a reduction in kainate-induced neuronal injury. While inhibition of protein kinase C (PKC) by staurosporin induced neurotoxicity, that was blocked by complestatin. Activation of PKC by phorbol dibutyrate partially inhibited the kainate-induced neurotoxicity. These results suggest that complestatin may be used as an anti-excitotoxic agent and involved in the PKC activation contributing to inhibition of neurotoxicity.
Full Text
http://link.springer.com/article/10.1023/A%3A1014919531306
DOI
10.1023/A:1014919531306
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Tropica Medicine (열대의학교실) > 1. Journal Papers
Yonsei Authors
Shin, Myeong Heon(신명헌) ORCID logo https://orcid.org/0000-0001-8207-6110
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/143438
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