NDLI: Different pathways lead to mitochondrial fragmentation during apoptotic and excitotoxic cell death in primary neurons.

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Different pathways lead to mitochondrial fragmentation during apoptotic and excitotoxic cell death in primary neurons.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Young, Kenneth W. Piñon, Lucia G. P. Bampton, Edward T. W. Nicotera, Pierluigi
Description	Country affiliation: United kingdom Author Affiliation: Young KW ( MRC Toxicology Unit, University of Leicester, Leicester, LE1 9HN, UK. kwy1@le.ac.uk)
Abstract	Mitochondrial fragmentation is recognized to be an important event during the onset of apoptosis. In this current study, we have used single cell imaging to investigate the role of the mitochondrial fission protein DRP-1 on mitochondrial morphology and mitochondrial fragmentation in primary hippocampal neurons undergoing necrotic or apoptotic cell death. Treatment of neurons with 500 nM staurosporine (apoptosis) or 30 µM glutamate (l-Glu; excitotoxic necrosis) produced a fragmentation and condensation of mitochondria, which although occurred over markedly different time frames appeared broadly similar in appearance. In neurons exposed to an apoptotic stimuli, inhibiting DRP-1 activity using overexpression of the dominant negative DRP-1(K38A) slowed the rate of mitochondrial fragmentation and decreased total cell death when compared to overexpression of wild-type DRP-1. In contrast, responses to l-Glu appeared DRP-1 independent. Similarly, alterations in the fission/fusion state of the mitochondrial network did not alter mitochondrial Ca(2+) uptake or the ability of l-Glu to stimulate excitotoxic Ca(2+) overload. Finally, apoptosis-induced mitochondrial fragmentation was observed concurrent with recruitment of Bax to the mitochondrial membrane. In contrast, during glutamate excitotoxicity, Bax remained in the cytosolic compartment. We conclude that different pathways lead to the appearance of fragmented mitochondria during necrotic and apoptotic neuronal cell death.
File Format	HTM / HTML
ISSN	10956670
Issue Number	5
Volume Number	24
e-ISSN	10990461
Journal	Journal of Biochemical and Molecular Toxicology
Language	English
Publisher	Wiley
Publisher Date	2010-09-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Molecular Biology Discipline Biochemistry Discipline Toxicology Apoptosis Physiology Mitochondria Metabolism Neurons Animals Drug Effects Calcium Cell Death Cells, Cultured Glutamic Acid Pharmacology Hippocampus Cytology Necrosis Neurotoxins Plasmids Genetics Rats Staurosporine Transfection Bcl-2-associated X Protein Comparative Study Journal Article
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Medicine Molecular Biology Biochemistry Toxicology Molecular Medicine

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