Complestatin antagonizes the AMPA/kainate-induced neurotoxicity in cultured chick telencephalic neurons

Neurochemical Research

Volumn 27, Issue 4, 2002, Pages 337-343

  Yoo, I D ^a   Yun, B S ^a   Ryoo, I J ^b   Lee, S Y ^b   Shin, M H ^c   Oh, S ^d  

^a Korea Research Institute of Bioscience and Biotechnology (KRIBB)   (South Korea)

^b Ewha Womans University   (South Korea)

^c Yonsei University College of Medicine   (South Korea)

^d Ewha Womans University School of Medicine   (South Korea)

Author keywords

AMPA kainite; Chick neuron; Complestatin; Neurotoxicity

Indexed keywords

6,7 DINITRO 2,3 QUINOXALINEDIONE; ALPHA AMINO 3 HYDROXY 5 METHYL 4 ISOXAZOLEPROPIONIC ACID; AMPA RECEPTOR ANTAGONIST; COMPLESTATIN; CYCLOTHIAZIDE; KAINIC ACID; KAINIC ACID RECEPTOR ANTAGONIST; PHORBOL DIBUTYRATE; PROTEIN KINASE C; STAUROSPORINE;

ANIMAL CELL; ARTICLE; CELL CULTURE; CHICK EMBRYO; CONCENTRATION RESPONSE; CONTROLLED STUDY; EMBRYO; ENZYME ACTIVATION; ENZYME INHIBITION; NERVE CELL; NERVE CELL LESION; NEUROPROTECTION; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; TELENCEPHALON;

ALPHA-AMINO-3-HYDROXY-5-METHYL-4-ISOXAZOLEPROPIONIC ACID; ANIMALS; CELLS, CULTURED; CHICK EMBRYO; CHICKENS; CHLOROPHENOLS; EXCITATORY AMINO ACID ANTAGONISTS; KAINIC ACID; NEURONS; OLIGOPEPTIDES; PEPTIDES, CYCLIC; PHORBOL 12,13-DIBUTYRATE; QUINOXALINES; RECEPTORS, AMPA; RECEPTORS, KAINIC ACID; STAUROSPORINE; TELENCEPHALON; TIME FACTORS;

ANIMALIA; STREPTOMYCES;

EID: 0036208309     PISSN: 03643190     EISSN: None     Source Type: Journal    
DOI: 10.1023/A:1014919531306     Document Type: Article

References (43)

1. Glutamate and the pathology of hypoxic-ischemic brain damage
2. Excitatory amino acids in epilepsy and potential novel theraphies
3. Excitotoxicity and the NMDA receptor
4. Excitotoxicity in neuro-degenerative disorders
5. Excitatory amino aicid neurotoxicity and neurodegenerative disease
6. 2+ influx into striatal neurons by kainic acid
7. Nifedipine attenuates slow excitatory amino acid neurotoxicity
8. Kainic acid: Neurophysiological and neurotoxic actions
9. Intraventricular kainic acid preferentially destroys hippocampal pyramidal cells
10. 3H]kainic acid binding sites in rat CNS as determined by autoradiography
11. Protection by NMDA antagonists against selective cell loss following transient ischaemia
12. 2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo (F)quinoxaline: A neuroprotectant for cerebral ischemia
13. Treatment with an AMPA antagonist 12 hours following severe normothermic forebrain ischemia prevents CA 1 neuronal injury
14. Inhibition of the alternative pathway of human complement in vitro by a natural microbial product, complestatin
15. A muscle-derived factor antagonizes the neurotoxicity of glutamate in dissociated cell cultures of chick telencephalic neurons
16. A series of normal stages in the development of the chick embryos
17. Multiple-conductance channels activated by excitatory amino acids in cerebellar neurons
18. Glutamate activates multiple single channel conductance in hippocampal neurons
19. Excitatory amino acid receptors in the brain: Membrane binding and receptor autoradiographic approaches
20. A family of AMPA selective glutamate receptors
21. Modulation of excitatory synaptic transmission by drugs that reduce desensitization at AMPA/kainate receptors
22. Hippocampal neurons exhibit cyclothizide-sensitive rapidly desensitising responses to kainate
23. Do NMDA antagonists protect against cerebral ischemia: Are clinical trials warranted?
24. Protection against ischemic neuronal damage by drugs acting on excitatory neurotransmission
25. Antagonism of the NMDA and non-NMDA receptors in global versus focal brain ischemia
26. Delayed AMPA receptor blockade reduces cerebral infarction by focal ischemia
27. Calpain I activation is specifically related to excitatory amino acid induction of hippocampal damage
28. Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures
29. NMDA-dependent superoxide production and neurotoxicity
30. NMDA receptors activate the arachidonic acid cascade system in spatial neurones
31. Excitotoxicity affects membrane potential and calmodulin kinase II activity in cultured rat cortical neurons
32. Outgrowth-regulating actions of glutamate in isolated hippocampal pyramidal neurons
33. Selective stimulation of excitatory amino acid receptor subtypes and survival of cerebellar granule cells in culture: Effect of kainic acid
34. Voltage regulated calcium channels involved in the regulation of enkephalin synthesis are blocked by phorbol ester
35. 2+-regulated transcription factor phosphorylated by calmodulin-dependent kinases
36. Regulation of neurite outgrowth from cerebellar granule cells in culture: NMDA receptors and protein kinase C
37. Evidence that the early loss of membrane protein kinase C is a necessary step in the excitatory amino acid-induced death of primary cortical neurons
38. How protein kinase C activation protects nerve cells from oxidative stress-induced cell death
39. Isozymes of protein kinase C: Differential involvement in apoptosis and pathogenesis
40. 2-induced apoptosis in CHO cells
41. Proteolytic activation of protein kinase C delta by an ICE/CED 3-like protease induces characteristics of apoptosis
42. Protein kinase Cδ targets mitochondria, alters mitochondrial membrane potential, and induces apoptosis is normal and neoplastic keratinocytes when overexpressed by an adenoviral vector
43. Complestatin is a noncompetitive peptide antagonist of N-methyl-D-aspartate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropioinic acid/kainite receptors: Secure blockade of ischemic neuronal death