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

Elena Petroff, Nathan Brot, Herbert Weissbach, Stefan H. Heinemann, Toshinori Hoshi

Research output: Contribution to journalArticleResearchpeer-review

82 Citations (Scopus)

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 Ca2+ signaling that is reversed by hypoxia. This potentiation critically depends on NO production and involves cellular ROS utilization. The ability to develop the Ca2+ signal potentiation is regulated by the developmental stage of nerve tissue, decreasing markedly in adult rat cortical neurons and differentiated PC12 cells.

Original languageEnglish
Pages (from-to)448-453
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume97
Issue number1
DOIs
StatePublished - 4 Jan 2000

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Neuronal Plasticity
Calcium Signaling
PC12 Cells
Reactive Oxygen Species
Nitric Oxide
Nerve Tissue
Signal Transduction
Neurons
Brain
Hypoxia

Cite this

Petroff, Elena ; Brot, Nathan ; Weissbach, Herbert ; Heinemann, Stefan H. ; Hoshi, Toshinori. / Reactive oxygen species and nitric oxide mediate plasticity of neuronal calcium signaling. In: Proceedings of the National Academy of Sciences of the United States of America. 2000 ; Vol. 97, No. 1. pp. 448-453.
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Reactive oxygen species and nitric oxide mediate plasticity of neuronal calcium signaling. / Petroff, Elena; Brot, Nathan; Weissbach, Herbert; Heinemann, Stefan H.; Hoshi, Toshinori.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 97, No. 1, 04.01.2000, p. 448-453.

Research output: Contribution to journalArticleResearchpeer-review

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