Publication Date:
1997-10-06
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C H -- Sensi, S L -- Gwag, B J -- Canzoniero, L M -- Farhangrazi, Z S -- Ying, H S -- Tian, M -- Dugan, L L -- Choi, D W -- 30337/PHS HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311914" target="_blank"〉PubMed〈/a〉
Keywords:
Amino Acid Chloromethyl Ketones/pharmacology
;
Animals
;
*Apoptosis/drug effects
;
Benzopyrans/pharmacology
;
Calcium/metabolism
;
Cerebral Cortex/cytology
;
Cromakalim
;
Cycloheximide/pharmacology
;
Cysteine Proteinase Inhibitors/pharmacology
;
Gadolinium/pharmacology
;
Mice
;
N-Methylaspartate/pharmacology
;
Neurons/*cytology/metabolism
;
Neuroprotective Agents/pharmacology
;
Nifedipine/pharmacology
;
Patch-Clamp Techniques
;
Potassium/*metabolism
;
Potassium Channels/drug effects/*metabolism
;
Pyrroles/pharmacology
;
Staurosporine/pharmacology
;
Tetraethylammonium
;
Tetraethylammonium Compounds/pharmacology
;
Veratridine/pharmacology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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