The Pyruvate Dehydrogenase Complex Is Partially Inactivated During Early Recirculation Following Short‐Term Forebrain Ischemia in Rats

: The mechanisms of selective neuronal loss after short‐term global ischemia remain undefined, but processes including increased proteolytic activity, impaired protein synthesis, and oxidative damage have been proposed to contribute. A decrease in activity of the pyruvate dehydrogenase complex in th...

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Bibliographic Details
Published in:Journal of neurochemistry 1998-01, Vol.70 (1), p.233-241
Main Authors: Zaidan, Emad, Sheu, Kwan‐Fu Rex, Sims, Neil R.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cerebral Cortex - enzymology
Corpus Striatum - enzymology
Enzyme Activation
Ischemia
Ischemic Attack, Transient - enzymology
Isoenzymes - metabolism
Male
Medical sciences
Mitochondria
Mitochondria - enzymology
Neurology
Neuronal death
Pyruvate dehydrogenase complex
Pyruvate Dehydrogenase Complex - metabolism
Rats
Rats, Inbred Strains
Reperfusion
Selective vulnerability
Time Factors
Vascular diseases and vascular malformations of the nervous system
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Summary:: The mechanisms of selective neuronal loss after short‐term global ischemia remain undefined, but processes including increased proteolytic activity, impaired protein synthesis, and oxidative damage have been proposed to contribute. A decrease in activity of the pyruvate dehydrogenase complex in the dorsolateral striatum, an ischemia‐susceptible region, is one change apparently differentiating this region from ischemia‐resistant areas during early recirculation. To provide an insight into processes contributing to postischemic cell damage, the changes in the pyruvate dehydrogenase complex during early recirculation have been further characterized. These studies provide clear confirmation that the activity of the pyruvate dehydrogenase complex is reduced in mitochondria from the dorsolateral striatum by 3 h of recirculation. The decrease in activity was not accompanied by a loss of antigenic sites or by changes in electrophoretic mobility of the components of the complex. A reduction in activity of the E1 component of the complex (39–42% decrease), but not the E2 and E3 components, was observed that was apparently sufficient to explain the decrease in activity of the whole complex. These results indicate that the changes in activity of the pyruvate dehydrogenase complex in the dorsolateral striatum are not due to loss or gross disruption of the constituent proteins but rather most likely reflect a selective inactivation of a specific component of the complex.
ISSN:0022-3042
1471-4159
DOI:10.1046/j.1471-4159.1998.70010233.x