Zn2+ Inhibits Mitochondrial Movement in Neurons by Phosphatidylinositol 3-Kinase Activation

Mitochondria have been identified as targets of the neurotoxic actions of zinc, possibly through decreased mitochondrial energy production and increased reactive oxygen species accumulation. It has been hypothesized that impairment of mitochondrial trafficking may be a mechanism of neuronal injury....

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Bibliographic Details
Published in:The Journal of neuroscience 2005-10, Vol.25 (41), p.9507-9514
Main Authors: Malaiyandi, Latha M, Honick, Anthony S, Rintoul, Gordon L, Wang, Qiming J, Reynolds, Ian J
Format: Article
Language:English
Subjects:
Animals
Cations, Divalent
Cells, Cultured
Cellular/Molecular
Chlorides - pharmacology
Chlorides - physiology
Dose-Response Relationship, Drug
Enzyme Activation - drug effects
Enzyme Activation - physiology
Mitochondria - drug effects
Mitochondria - enzymology
Neural Inhibition - drug effects
Neural Inhibition - physiology
Neurons - drug effects
Neurons - enzymology
Phosphatidylinositol 3-Kinases - metabolism
Rats
Rats, Sprague-Dawley
Zinc - pharmacology
Zinc - physiology
Zinc Compounds - pharmacology
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Summary:Mitochondria have been identified as targets of the neurotoxic actions of zinc, possibly through decreased mitochondrial energy production and increased reactive oxygen species accumulation. It has been hypothesized that impairment of mitochondrial trafficking may be a mechanism of neuronal injury. Here, we report that elevated intraneuronal zinc impairs mitochondrial trafficking. At concentrations just sufficient to cause injury, zinc rapidly inhibited mitochondrial movement without altering morphology. Zinc chelation initially restored movement, but the actions of zinc became insensitive to chelator in
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.0868-05.2005