| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6022854 | Neurobiology of Disease | 2011 | 10 Pages |
Abstract
⺠Repetitive nerve stimulation transiently depolarizes mitochondria in motor terminals. ⺠This Ψm depolarization increases in symptomatic fALS mice (SOD1-G93A, -G85R). ⺠Cyclosporin A or substitution of Sr2+ for Ca2+ reduces these large Ψm depolarizations. ⺠Diamide increases stimulation-evoked Ψm depolarizations in wild-type mice. ⺠Mitochondrial transition pore openings may contribute to motor terminal degeneration.
Keywords
Cu/Zn superoxide dismutase 1LALDAPMPTPSOD1familial amyotrophic lateral sclerosismitochondrial permeability transition poreCSAMotor nerve terminalOxidative stressMitochondrial calcium uptakefALSDiaminopyridineRh-123Rhodamine 123electron transport chaincyclosporin AMitochondriaMotor neuronETcMitochondrial membrane potentialΨm
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Authors
Khanh T. Nguyen, John N. Barrett, Luis GarcÃa-Chacón, Gavriel David, Ellen F. Barrett,