Reactive oxygen species and nitric oxide mediate plasticity of neuronal calcium signaling

Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):448-53. doi: 10.1073/pnas.97.1.448.

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

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Brain / metabolism
  • Calcium Signaling / drug effects*
  • Cell Differentiation
  • Fura-2 / metabolism
  • Histamine / pharmacology
  • Hydrogen Peroxide / pharmacology
  • Hypoxia / metabolism
  • Methionine Sulfoxide Reductases
  • Nerve Growth Factor / pharmacology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Nitric Oxide / metabolism*
  • Nitroprusside / pharmacology
  • Oxidoreductases / metabolism
  • Oxygen / metabolism
  • PC12 Cells
  • Potassium / pharmacology
  • Rats
  • Reactive Oxygen Species / metabolism
  • Signal Transduction

Substances

  • Reactive Oxygen Species
  • Nitroprusside
  • Nitric Oxide
  • Histamine
  • Nerve Growth Factor
  • Hydrogen Peroxide
  • Oxidoreductases
  • Methionine Sulfoxide Reductases
  • methionine sulfoxide reductase
  • Potassium
  • Oxygen
  • Fura-2