Work

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

Year: 2000

Type: article

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.

Source: Proceedings of the National Academy of Sciences

DOI: 10.1073/pnas.97.1.448

Authors: Olena Yermolaieva, Nathan Brot, Herbert Weissbach, Stefan H. Heinemann, Toshinori Hoshi

Institutions: University of Iowa, Hospital for Special Surgery, Cornell University, Florida Atlantic University, Friedrich Schiller University Jena

Language: English

Topic: Neuroscience and Neuropharmacology Research

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

Open Access status: green

Funders: Deutsche Forschungsgemeinschaft, National Institutes of Health, National Heart, Lung, and Blood Institute, National Institute of General Medical Sciences

Awards: G320453980, Regulation of calcium-activated potassium channels by lipid messengers, G4599204049, Integrative Neurobiology of Cardiovascular Regulation, G9000076741