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Mediation of neuronal apoptosis by enhancement of outward potassium current.

Authors
Yu, SP; Yeh, CH; Sensi, SL; Gwag, BJ; Canzoniero, LM; Farhangrazi, ZS; Ying, HS; Tian, M; Dugan, LL; Choi, DW
Citation
Science, 278(5335):114-117, 1997
Journal Title
Science
ISSN
0193-4511
Abstract
Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (IK) current and loss of total intracellular K+. This IK augmentation was not seen in neurons undergoing excitotoxic necrosis or in older neurons resistant to staurosporine-induced apoptosis. Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented. Furthermore, exposure to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis. Enhanced K+ efflux may mediate certain forms of neuronal apoptosis.
MeSH terms
Amino Acid Chloromethyl Ketones/pharmacologyAnimals*Apoptosis/drug effectsBenzopyrans/pharmacologyCalcium/metabolismCerebral Cortex/cytologyCromakalimCycloheximide/pharmacologyCysteine Proteinase Inhibitors/pharmacologyGadolinium/pharmacologyMiceN-Methylaspartate/pharmacologyNeurons/*cytology/metabolismNeuroprotective Agents/pharmacologyNifedipine/pharmacologyPatch-Clamp TechniquesPotassium/*metabolismPotassium Channels/drug effects/*metabolismPyrroles/pharmacologyStaurosporine/pharmacologyTetraethylammonium
PMID
9311914
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
곽, 병주
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