Linked Life Data

18205748

Source:http://linkedlifedata.com/resource/pubmed/id/18205748

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-4-23
pubmed:abstractText
The Alamar blue (resazurin) assay of cell viability monitors the irreversible reduction of non-fluorescent resazurin to fluorescent resorufin. This study focused on the reversible reduction of C12-resorufin to non-fluorescent C12-dihydroresorufin in motor nerve terminals innervating lizard intercostal muscles. Resting C12-resorufin fluorescence decreased when the activity of the mitochondrial electron transport chain (ETC) was accelerated with carbonyl cyanide m-chloro phenyl hydrazone, and increased when ETC activity was inhibited with cyanide. Trains of action potentials (50 Hz for 20-50 s), which reversibly decreased NADH fluorescence and partially depolarized the mitochondrial membrane potential, produced a reversible decrease in C12-resorufin fluorescence which had a similar time course. The stimulation-induced decrease in C12-resorufin fluorescence was blocked by inhibitors of ETC complexes I, III, and IV and by carbonyl cyanide m-chloro phenyl hydrazone, but not by inhibiting mitochondrial ATP synthesis with oligomycin. Mitochondrial depolarization and the decreases in C12-resorufin and NADH fluorescence depended on Ca2+ influx into the terminal, but not on vesicular transmitter release. These results suggest that the reversible reduction of C12-resorufin in stimulated motor nerve terminals is linked, directly or indirectly, to the reversible oxidation of NADH and to Ca(2+) influx into mitochondria, and provides an assay for rapid changes in motor terminal metabolism.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1471-4159
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
807-19
pubmed:meshHeading
pubmed-meshheading:18205748-Action Potentials, pubmed-meshheading:18205748-Animals, pubmed-meshheading:18205748-Biological Assay, pubmed-meshheading:18205748-Calcium Signaling, pubmed-meshheading:18205748-Carbon Isotopes, pubmed-meshheading:18205748-Electron Transport Chain Complex Proteins, pubmed-meshheading:18205748-Energy Metabolism, pubmed-meshheading:18205748-Fluorescence, pubmed-meshheading:18205748-Indicators and Reagents, pubmed-meshheading:18205748-Lizards, pubmed-meshheading:18205748-Microscopy, Fluorescence, pubmed-meshheading:18205748-Mitochondria, pubmed-meshheading:18205748-Motor Neurons, pubmed-meshheading:18205748-NAD, pubmed-meshheading:18205748-Neurochemistry, pubmed-meshheading:18205748-Neuromuscular Junction, pubmed-meshheading:18205748-Oxazines, pubmed-meshheading:18205748-Oxidation-Reduction, pubmed-meshheading:18205748-Presynaptic Terminals, pubmed-meshheading:18205748-Uncoupling Agents
pubmed:year
2008
pubmed:articleTitle
Rapid, stimulation-induced reduction of C12-resorufin in motor nerve terminals: linkage to mitochondrial metabolism.
pubmed:affiliation
Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, Miami, Florida 33101, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural