| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6018849 | Experimental Neurology | 2012 | 10 Pages |
Abstract
⺠An oxygen/glucose deprivation stress was applied to mouse neuromuscular preparations. ⺠This stress elevated [Ca2 +] and depolarized mitochondria within motor terminals. ⺠Removal of bath Ca2 + during the stress preserved motor terminals and axons. ⺠Inhibitors of Ca2 + influx and of calpain activation preserved endplate innervation. ⺠Motor terminal degeneration following oxygen/glucose deprivation is Ca2 +-dependent.
Keywords
α-BgTxNa+/Ca2 + exchangerLALOGDYFPEDLSOD1NKCC1alpha-bungarotoxin1,2-Bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acidI/Roxygen/glucose deprivationischemia/reperfusionBAPTAMotor nerve terminalRh-123Rhodamine 123superoxide dismutase 1Extensor digitorum longus muscleOxygen-glucose deprivationMousewild-typeHypoxiayellow fluorescent proteinΨmCalpainCalcium
Related Topics
Life Sciences
Neuroscience
Neurology
Authors
Janet D. Talbot, Gavriel David, Ellen F. Barrett, John N. Barrett,