Raising intracellular calcium attenuates neuronal apoptosis triggered by staurosporine or oxygen-glucose deprivation in the presence of glutamate receptor blockade

Lorella M.T. Canzoniero, Debra J. Babcock, Frank J. Gottron, Margaret C. Grabb, Pat Manzerra, B. Joy Snider, Dennis W. Choi

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

The relationship between intracellular Ca2+ ([Ca 2+]i) regulation and programmed cell death is not well-defined; both increases and decreases in [Ca2+]i have been observed in cells undergoing apoptosis. We determined [Ca 2+]i in cultured murine cortical neurons undergoing apoptosis after exposure to staurosporine or following oxygen-glucose deprivation in the presence of glutamate receptor antagonists. Neuronal [Ca 2+]i was decreased 1-4 h after exposure to staurosporine (30 nM). A [Ca2+]i decrease was also observed 1 h after the end of the oxygen-glucose deprivation period when MK-801 and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) were added to the bathing medium during the deprivation period. A similar decrease in [Ca2+] i produced by reducing extracellular Ca2+ or chelating intracellular Ca2+ was sufficient to induce neuronal apoptosis. Raising [Ca2+]i either by activating voltage-sensitive Ca2+ channels with (-) Bay K8644 or by application of low concentrations of kainate attenuated both staurosporine and oxygen-glucose deprivation-induced apoptosis.

Original languageEnglish
Pages (from-to)520-528
Number of pages9
JournalNeurobiology of Disease
Volume15
Issue number3
DOIs
StatePublished - Apr 1 2004

Keywords

  • Apoptosis
  • Calcium
  • Staurosporine

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