Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1997-3-26
pubmed:abstractText
N-Methyl-D-aspartate causes a rapid increase in intracellular Ca2+ leading to collapse of the mitochondrial membrane potential and eventually cell death in cortical neurons. The aim of this study was to investigate the mechanism responsible for mitochondrial depolarization using laser scanning confocal microscopy of single cultured rate cortical neurons. To monitor mitochondrial membrane potential, neuronal mitochondria were labeled with tetramethylrhodamine methyl ester, a cationic fluorophore that accumulates in polarized mitochondria. In neurons cultured on poly-D-lysine-coated coverslips, N-methyl-D-aspartate caused mitochondrial depolarization in 88% of cells in 30 min. Cyclosporin A, an inhibitor of the mitochondrial permeability transition, delayed depolarization in a dose-dependent manner (0.2-1 microM). In neurons cultured on an astrocyte feeder layer, N-methyl-D-aspartate also caused mitochondrial depolarization. Cyclosporin A again delayed mitochondrial depolarization, although higher concentrations were needed. These data show for the first time that mitochondrial depolarization induced by N-methyl-D-aspartate may be due to the induction of the mitochondrial permeability transition.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
993-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Cyclosporin A delays mitochondrial depolarization induced by N-methyl-D-aspartate in cortical neurons: evidence of the mitochondrial permeability transition.
pubmed:affiliation
Department of Anatomy, School of Medicine, Case Western Reserve University, Cleveland, OH 44106-4930, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't