 |
Previous Article | Next Article 
Journal of Neuroscience, Vol 13, 623-631, Copyright © 1993 by Society for Neuroscience
Intracellular calcium levels during the period of delayed excitotoxicity
JM Dubinsky
Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756.
Intracellular calcium concentrations ([Ca2+]i) among cultured hippocampal
neurons were monitored during and in the hours following an excitotoxic
glutamate application to determine the time course of changes involved in
delayed excitotoxicity. After a 5 min toxic insult, [Ca2+]i increased
immediately and remained elevated for an hour. Subsequently, [Ca2+]i
declined to normal resting levels and remained so up to 13 hr following
insult. Only a few neurons displayed greatly elevated [Ca2+]i at these
extended times. Survival experiments in sister cultures indicated that 85%
of the neurons died after 24 hr. Therefore, intracellular calcium returned
to baseline levels prior to neuronal death. Additionally, during this
period when basal calcium levels had recovered, the majority of neurons
responded to a second excitatory amino acid application with a second
increase in [Ca2+]i.
This article has been cited by other articles:

|
 |

|
 |
 
L. S. Deshpande, D. D. Limbrick Jr., S. Sombati, and R. J. DeLorenzo
Activation of a Novel Injury-Induced Calcium-Permeable Channel That Plays a Key Role in Causing Extended Neuronal Depolarization and Initiating Neuronal Death in Excitotoxic Neuronal Injury
J. Pharmacol. Exp. Ther.,
August 1, 2007;
322(2):
443 - 452.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. Shalbuyeva, T. Brustovetsky, A. Bolshakov, and N. Brustovetsky
Calcium-dependent Spontaneously Reversible Remodeling of Brain Mitochondria
J. Biol. Chem.,
December 8, 2006;
281(49):
37547 - 37558.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
C. M. Norris, E. M. Blalock, O. Thibault, L. D. Brewer, G. V. Clodfelter, N. M. Porter, and P. W. Landfield
Electrophysiological Mechanisms of Delayed Excitotoxicity: Positive Feedback Loop Between NMDA Receptor Current and Depolarization-Mediated Glutamate Release
J Neurophysiol,
November 1, 2006;
96(5):
2488 - 2500.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. B. Pivovarova, H. V. Nguyen, C. A. Winters, C. A. Brantner, C. L. Smith, and S. B. Andrews
Excitotoxic Calcium Overload in a Subpopulation of Mitochondria Triggers Delayed Death in Hippocampal Neurons
J. Neurosci.,
June 16, 2004;
24(24):
5611 - 5622.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A. Lakkaraju, Y.-E. Rahman, and J. M. Dubinsky
Low-density Lipoprotein Receptor-related Protein Mediates the Endocytosis of Anionic Liposomes in Neurons
J. Biol. Chem.,
April 19, 2002;
277(17):
15085 - 15092.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
C. W. R. Shuttleworth and J. A. Connor
Strain-Dependent Differences in Calcium Signaling Predict Excitotoxicity in Murine Hippocampal Neurons
J. Neurosci.,
June 15, 2001;
21(12):
4225 - 4236.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. Brustovetsky and J. M. Dubinsky
Limitations of Cyclosporin A Inhibition of the Permeability Transition in CNS Mitochondria
J. Neurosci.,
November 15, 2000;
20(22):
8229 - 8237.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. W. Ward, A. C. Rego, B. G. Frenguelli, and D. G. Nicholls
Mitochondrial Membrane Potential and Glutamate Excitotoxicity in Cultured Cerebellar Granule Cells
J. Neurosci.,
October 1, 2000;
20(19):
7208 - 7219.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. A. Connor and R. J. Cormier
Cumulative Effects of Glutamate Microstimulation on Ca2+ Responses of CA1 Hippocampal Pyramidal Neurons in Slice
J Neurophysiol,
January 1, 2000;
83(1):
90 - 98.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. L. Sensi, H. Z. Yin, S. G. Carriedo, S. S. Rao, and J. H. Weiss
Preferential Zn2+ influx through Ca2+-permeable AMPA/kainate channels triggers prolonged mitochondrial superoxide production
PNAS,
March 2, 1999;
96(5):
2414 - 2419.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. A. Connor, S. Razani-Boroujerdi, A. C. Greenwood, R. J. Cormier, J. J. Petrozzino, and R. C. S. Lin
Reduced Voltage-Dependent Ca2+ Signaling in CA1 Neurons After Brief Ischemia in Gerbils
J Neurophysiol,
January 1, 1999;
81(1):
299 - 306.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. G. Carriedo, H. Z. Yin, S. L. Sensi, and J. H. Weiss
Rapid Ca2+ Entry through Ca2+-Permeable AMPA/Kainate Channels Triggers Marked Intracellular Ca2+ Rises and Consequent Oxygen Radical Production
J. Neurosci.,
October 1, 1998;
18(19):
7727 - 7738.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
K. Hyrc, S. D. Handran, S. M. Rothman, and M. P. Goldberg
Ionized Intracellular Calcium Concentration Predicts Excitotoxic Neuronal Death: Observations with Low-Affinity Fluorescent Calcium Indicators
J. Neurosci.,
September 1, 1997;
17(17):
6669 - 6677.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
P. Sammak, L. Hinman, P. Tran, M. Sjaastad, and T. Machen
How do injured cells communicate with the surviving cell monolayer?
J. Cell Sci.,
January 2, 1997;
110(4):
465 - 475.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
Y. M. Lu, H. Z. Yin, J. Chiang, and J. H. Weiss
Ca2+-Permeable AMPA/Kainate and NMDA Channels: High Rate of Ca2+ Influx Underlies Potent Induction of Injury
J. Neurosci.,
September 1, 1996;
16(17):
5457 - 5465.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A. Lakkaraju, J. M. Dubinsky, W. C. Low, and Y.-E. Rahman
Neurons Are Protected from Excitotoxic Death by p53 Antisense Oligonucleotides Delivered in Anionic Liposomes
J. Biol. Chem.,
August 17, 2001;
276(34):
32000 - 32007.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|

|