Abstract
Reactive oxygen species (ROS) and nitric oxide (NO) are important participants in signal transduction that could provide the cellular basis for activity-dependent regulation of neuronal excitability. In young rat cortical brain slices and undifferentiated PC12 cells, paired application of depolarization/agonist stimulation and oxidation induces long-lasting potentiation of subsequent Ca(2+) signaling that is reversed by hypoxia. This potentiation critically depends on NO production and involves cellular ROS utilization. The ability to develop the Ca(2+) signal potentiation is regulated by the developmental stage of nerve tissue, decreasing markedly in adult rat cortical neurons and differentiated PC12 cells.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Brain / metabolism
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Calcium Signaling / drug effects*
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Cell Differentiation
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Fura-2 / metabolism
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Histamine / pharmacology
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Hydrogen Peroxide / pharmacology
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Hypoxia / metabolism
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Methionine Sulfoxide Reductases
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Nerve Growth Factor / pharmacology
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Neurons / drug effects
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Neurons / metabolism*
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Nitric Oxide / metabolism*
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Nitroprusside / pharmacology
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Oxidoreductases / metabolism
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Oxygen / metabolism
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PC12 Cells
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Potassium / pharmacology
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Rats
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Reactive Oxygen Species / metabolism
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Signal Transduction
Substances
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Reactive Oxygen Species
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Nitroprusside
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Nitric Oxide
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Histamine
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Nerve Growth Factor
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Hydrogen Peroxide
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Oxidoreductases
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Methionine Sulfoxide Reductases
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methionine sulfoxide reductase
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Potassium
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Oxygen
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Fura-2