Complestatin is a noncompetitive peptide antagonist of N-methyl-D-aspartate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptors : secure blockade of ischemic neuronal death

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Title
Complestatin is a noncompetitive peptide antagonist of N-methyl-D-aspartate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptors : secure blockade of ischemic neuronal death
Author(s)
So Young Seo; Bong Sik Yun; In Ja Ryoo; Jun Sub Choi; Choun Ki Joo; Su Youne Chang; Jun Mo Chung; Sei Kwan Oh; Byoung Joo Gwag; Ick Dong Yoo
Bibliographic Citation
Journal of Pharmacology and Experimental Therapeutics, vol. 299, no. 1, pp. 377-384
Publication Year
2001
Abstract
Complestatin, a peptide derived from Streptomyces, was found to protect cultured cortical neurons from excitotoxicity induced by N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), or kainate. This neuroprotective behavior of complestatin was attributed to a blockade of Ca2+ ion entry and accumulation, after the activation of NMDA and AMPA/kainate receptors. Complestatin reversibly interfered with NMDA- and AMPA-mediated excitatory synaptic transmission. Complestatin also protected cortical neurons from prolonged deprivation of oxygen and glucose, more effectively than combined antagonists of NMDA and AMPA/kainate receptors. Neurotoxicity, evolving within 1 to 2 days after continuous exposure to combined NMDA and AMPA/kainate antagonists, was not observed in cortical cell cultures that were exposed to complestatin. Finally, complestatin dose dependently prevented neuronal death evolving within the inner nuclear and ganglion cell layers, after transient retinal ischemia. We conclude that complestatin possesses novel pharmacological properties that effectively prevent excitotoxicity under certain pathological conditions.
ISSN
0022-3565
Publisher
Amer Soc Pharmacology Experimental Therapeutics
Type
Article
Appears in Collections:
Ochang Branch Institute > Chemical Biology Research Center > 1. Journal Articles
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