Mediation of neuronal apoptosis by enhancement of outward potassium current

Shan Ping Yu, Chen Hsiung Yeh, Stefano L. Sensi, Byoung J. Gwag, Lorella M T Canzoniero, Z. Shadi Farhangrazi, Howard S. Ying, Min Tian, Laura L. Dugan, Dennis W. Choi

Research output: Contribution to journalArticle

Abstract

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

Original languageEnglish (US)
Pages (from-to)114-117
Number of pages4
JournalScience
Volume278
Issue number5335
DOIs
StatePublished - Oct 3 1997
Externally publishedYes

Fingerprint

Potassium
Apoptosis
Staurosporine
Neurons
Cromakalim
Valinomycin
Tetraethylammonium
Ionophores
Necrosis
Serum

ASJC Scopus subject areas

  • General

Cite this

Yu, S. P., Yeh, C. H., Sensi, S. L., Gwag, B. J., Canzoniero, L. M. T., Farhangrazi, Z. S., ... Choi, D. W. (1997). Mediation of neuronal apoptosis by enhancement of outward potassium current. Science, 278(5335), 114-117. https://doi.org/10.1126/science.278.5335.114

Mediation of neuronal apoptosis by enhancement of outward potassium current. / Yu, Shan Ping; Yeh, Chen Hsiung; Sensi, Stefano L.; Gwag, Byoung J.; Canzoniero, Lorella M T; Farhangrazi, Z. Shadi; Ying, Howard S.; Tian, Min; Dugan, Laura L.; Choi, Dennis W.

In: Science, Vol. 278, No. 5335, 03.10.1997, p. 114-117.

Research output: Contribution to journalArticle

Yu, SP, Yeh, CH, Sensi, SL, Gwag, BJ, Canzoniero, LMT, Farhangrazi, ZS, Ying, HS, Tian, M, Dugan, LL & Choi, DW 1997, 'Mediation of neuronal apoptosis by enhancement of outward potassium current', Science, vol. 278, no. 5335, pp. 114-117. https://doi.org/10.1126/science.278.5335.114
Yu SP, Yeh CH, Sensi SL, Gwag BJ, Canzoniero LMT, Farhangrazi ZS et al. Mediation of neuronal apoptosis by enhancement of outward potassium current. Science. 1997 Oct 3;278(5335):114-117. https://doi.org/10.1126/science.278.5335.114
Yu, Shan Ping ; Yeh, Chen Hsiung ; Sensi, Stefano L. ; Gwag, Byoung J. ; Canzoniero, Lorella M T ; Farhangrazi, Z. Shadi ; Ying, Howard S. ; Tian, Min ; Dugan, Laura L. ; Choi, Dennis W. / Mediation of neuronal apoptosis by enhancement of outward potassium current. In: Science. 1997 ; Vol. 278, No. 5335. pp. 114-117.
@article{2b9ea6ad1e654cc898057055cbe9fd84,
title = "Mediation of neuronal apoptosis by enhancement of outward potassium current",
abstract = "Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (l(K)) current and loss of total intracellular K+. This l(K) 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.",
author = "Yu, {Shan Ping} and Yeh, {Chen Hsiung} and Sensi, {Stefano L.} and Gwag, {Byoung J.} and Canzoniero, {Lorella M T} and Farhangrazi, {Z. Shadi} and Ying, {Howard S.} and Min Tian and Dugan, {Laura L.} and Choi, {Dennis W.}",
year = "1997",
month = "10",
day = "3",
doi = "10.1126/science.278.5335.114",
language = "English (US)",
volume = "278",
pages = "114--117",
journal = "Science",
issn = "0036-8075",
publisher = "American Association for the Advancement of Science",
number = "5335",

}

TY - JOUR

T1 - Mediation of neuronal apoptosis by enhancement of outward potassium current

AU - Yu, Shan Ping

AU - Yeh, Chen Hsiung

AU - Sensi, Stefano L.

AU - Gwag, Byoung J.

AU - Canzoniero, Lorella M T

AU - Farhangrazi, Z. Shadi

AU - Ying, Howard S.

AU - Tian, Min

AU - Dugan, Laura L.

AU - Choi, Dennis W.

PY - 1997/10/3

Y1 - 1997/10/3

N2 - Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (l(K)) current and loss of total intracellular K+. This l(K) 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.

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

UR - http://www.scopus.com/inward/record.url?scp=0000521423&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0000521423&partnerID=8YFLogxK

U2 - 10.1126/science.278.5335.114

DO - 10.1126/science.278.5335.114

M3 - Article

C2 - 9311914

AN - SCOPUS:0000521423

VL - 278

SP - 114

EP - 117

JO - Science

JF - Science

SN - 0036-8075

IS - 5335

ER -