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Mediation of Neuronal Apoptosis by Enhancement of Outward Potassium Current

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Science  03 Oct 1997:
Vol. 278, Issue 5335, pp. 114-117
DOI: 10.1126/science.278.5335.114

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Abstract

Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (I K) current and loss of total intracellular K+. This I Kaugmentation 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.

  • * To whom correspondence should be addressed at the Department of Neurology, Box 8111, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. E-mail: choid{at}neuro.wustl.edu

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