These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Raising intracellular calcium attenuates neuronal apoptosis triggered by staurosporine or oxygen-glucose deprivation in the presence of glutamate receptor blockade.
    Author: Canzoniero LM, Babcock DJ, Gottron FJ, Grabb MC, Manzerra P, Snider BJ, Choi DW.
    Journal: Neurobiol Dis; 2004 Apr; 15(3):520-8. PubMed ID: 15056459.
    Abstract:
    The relationship between intracellular Ca(2+) ([Ca(2+)](i)) regulation and programmed cell death is not well-defined; both increases and decreases in [Ca(2+)](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 [Ca(2+)](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 [Ca(2+)](i) produced by reducing extracellular Ca(2+) or chelating intracellular Ca(2+) was sufficient to induce neuronal apoptosis. Raising [Ca(2+)](i) either by activating voltage-sensitive Ca(2+) channels with (-) Bay K8644 or by application of low concentrations of kainate attenuated both staurosporine and oxygen-glucose deprivation-induced apoptosis.
    [Abstract] [Full Text] [Related] [New Search]