Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone.

Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone. Research Abstract Details 

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Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone. Abstract Text:

Nagendra Yadava,David G Nicholls,

Partial inhibition of mitochondrial respiratory complex I by rotenone reproduces aspects of Parkinson's disease in rodents. The hypothesis that rotenone enhancement of neuronal cell death is attributable to oxidative stress was tested in an acute glutamate excitotoxicity model using primary cultures of rat cerebellar granule neurons. As little as 5 nM rotenone increased mitochondrial superoxide (O2*-) levels and potentiated glutamate-induced cytoplasmic Ca2+ deregulation, the first irreversible stage of necrotic cell death. However, the potent cell-permeant O2*- trap manganese tetrakis (N-ethylpyridinium-2yl) porphyrin failed to prevent the effects of the inhibitor. The bioenergetic consequences of rotenone addition were quantified by monitoring cell respiration. Glutamate activation of NMDA receptors used the full respiratory capacity of the in situ mitochondria, and >80% of the glutamate-stimulated respiration was attributable to increased cellular ATP demand. Rotenone at 20 nM inhibited basal and carbonyl cyanide p-trifluoromethoxyphenylhydrazone-stimulated cell respiration and caused respiratory failure in the presence of glutamate. ATP synthase inhibition by oligomycin was also toxic in the presence of glutamate. We conclude that the cell vulnerability in the rotenone model of partial complex I deficiency under these specific conditions is primarily determined by spare respiratory capacity rather than oxidative stress.

Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone. Publishing Authors By Initials

N Yadava,DG Nicholls,

For similar heterocyclic compounds: heterocyclic compounds, 2-ring: benzopyrans: chromones: flavonoids: isoflavones: rotenone research abstracts see: heterocyclic compounds: heterocyclic compounds, 2-ring: benzopyrans: chromones: flavonoids: isoflavones: rotenone research

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Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The Journal of neuroscience : the official journal

VOLUME: 27

Page Numbers: 7310-7

Journal Abbreviation: J. Neurosci.

ISSN: 1529-2401

DAY: 4

MONTH: Jul

YEAR: 2007

Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone. Information

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LANGUAGE: eng

NlmUniqueID: 8102140

Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone. Keywords Mesh Terms:

KEYWORDS: Rotenone

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone. Information

Substance Name: Electron Transport Complex I

Registry Number: EC 1.6.5.3

Grant and Affiliation Information for Spare respiratory capacity rather than oxidative stress regulates glutamate excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone.

AFFILIATION: Buck Institute for Age Research, Novato, California 94945, USA.

Country: United States

AGENCY: United States NIA

GRANT: R01 AG2 1440

ACRONYM: AG

MEDLINETA: J Neurosci

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