Reactive Oxygen Species and Nitric Oxide Mediate Plasticity of Neuronal Calcium Signaling
Document Type
Article
Publication Date
1-4-2000
Journal / Book Title
Proceedings of the National Academy of Sciences of the United States of America
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.
DOI
10.1073/pnas.97.1.448
Montclair State University Digital Commons Citation
Petroff, Elena; Brot, Nathan; Weissbach, Herbert; Heinemann, Stefan H.; and Hoshi, Toshinori, "Reactive Oxygen Species and Nitric Oxide Mediate Plasticity of Neuronal Calcium Signaling" (2000). Department of Biology Faculty Scholarship and Creative Works. 231.
https://digitalcommons.montclair.edu/biology-facpubs/231
Published Citation
Yermolaieva, O., Brot, N., Weissbach, H., Heinemann, S. H., & Hoshi, T. (2000). Reactive oxygen species and nitric oxide mediate plasticity of neuronal calcium signaling. Proceedings of the National Academy of Sciences of the United States of America, 97(1), 448–453. https://doi.org/10.1073/pnas.97.1.448